The Cancer Code, Gene Reprogramming, & Searching for a Cure | Marc Malone

Summary

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Podcast Summary

Podcast: Matt Beall Podcast
Episode: The Cancer Code, Gene Reprogramming, & Searching for a Cure | Marc Malone
Date: July 9, 2026
Guest: Marc Malone
Host: Matt Beall

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Episode Overview

In this emotionally charged and deeply insightful conversation, Matt Beall interviews Marc Malone—a self-taught scientist and father whose relentless pursuit to save his wife and son from terminal diseases has led him to groundbreaking discoveries in gene reprogramming and cancer treatment. The discussion explores Marc’s journey from poverty-stricken beginnings to front-line innovation in molecular biology, detailing both personal heartbreak and revolutionary therapeutic advances. Marc shares the deeply personal stories behind his scientific mission, bridges philosophy and science, and outlines potential paths toward a future where genetic and degenerative diseases could be treatable or even reversible.

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Major Discussion Points & Insights

Marc’s Background & Motivation (03:12–10:39)

• Personal Adversity: Marc was raised in severe poverty in England, with a mentally ill father and chronically sick mother. Despite being considered "gifted," the school system disregarded him due to his circumstances.
  • "Just because you were born into an environment like that doesn't mean it has to define what you become." (04:39, Marc)
• Tragedy & Love: Endured losses, including a missing brother, Aaron, and later met his wife Jill—whose love inspired his personal growth and grounded his life.
• Family: Married Jill, raised three children—Aaron, Sky, and Iona—while dealing with the struggles of the COVID-19 pandemic and later, devastating medical diagnoses.

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The Diagnosis & Scientific Journey (11:57–18:34)

• Jill’s Cancer: In 2023, Jill was diagnosed with an ultra-lethal, treatment-resistant form of triple-negative breast cancer, compounded by rare genetic mutations. Prognosis: less than 1% survive three months.
• Immediate Action: Marc realized conventional medicine offered no hope, compelling him to self-educate on molecular biology and oncology, conceptualizing a "causal, not consequential" approach to disease (17:08).

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Gene Reprogramming Discovery (22:58–39:13)

The "Triune" Approach:

1. Molecule Selection: Used a re-engineered molecule from the Streptomyces/avermectin family (related to ivermectin) to "crack open" locked cancer cells.
2. Energy Starvation: Targeted cancer cell metabolism by depriving them of glucose and glutamine—crucial for rapid proliferation.
3. Intracellular Signaling: Manipulated cell signaling pathways to not just kill, but transform cancer cells.

• “We triggered receptors and genes back on in completely different chromosomes in completely different areas of the body… perhaps the first instance we've seen of cancer actively reversing." (26:55, Marc)
• Notable Moment: One metastatic tumor disappeared completely, and the primary tumor shrank by 70–77%. (27:16)

Philosophical Perspective:

• Marc likens his approach to the Constitution’s "via negativa" principle: remove suppressors rather than forcibly engineer outcomes.
• "All I did is remove locks… the genome itself is what restored itself." (34:19, Marc)

Limitations & Lessons Learned:

• The anti-cancer effect couldn’t be sustained because energy starvation harmed Jill’s healthy cells too.
• “We had the proof of concept… but after that point, she started to decline again because I couldn't sustain it.” (39:13, Marc)

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Pushing the Boundaries: Cancer Stem Cell Elimination (54:45–66:01)

• Breakthrough with Niclosamide: Using a re-engineered, bioavailable form of an old tapeworm drug (niclosamide), Marc managed to eliminate all detectable cancer stem cell pathways in Jill; tumors drastically shrank within a week.
  • “In the most ultra aggressive, lethal, treatment-resistant possible cancer case, the tumors halved in a week.” (59:09, Marc)
• Significance: Cancer stem cell pathways exist in all cancers—their elimination is the "closest to a cancer cure proven in a human we've ever had." (59:53, Marc)
• Perspective: This isn’t an outright cure, but "puts cancer in stasis," blocking recurrence and metastasis, allowing time for other therapies to function.

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Advocating for Broader Impact & Scientific Transparency (66:01–74:31)

• Current Barriers: Marc’s published proof-of-concept studies face skepticism due to lack of traditional IRB approval and institutional credentials.
  • “They wouldn’t accept it because I did a human case without a review board approving it.” (68:41, Marc)
• Need for Investment: Seeks mission-aligned funding for small patient trials and further gene reprogramming preclinical work, determined not to cede results to uninterested or unethical venture capitalists.

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The Next Mission: Saving His Son & Tackling Genetic Disease (77:37–100:33)

• Aaron’s Complex Case: His son suffers from severe autism, multiple rare mutations, and a "collapsing genome" with terminal outcomes predicted from multiple directions (cancer and ALS/Lou Gehrig’s).
  • "He's not really going to die of one disease, he's going to die of a dozen, as they're all starting to cave in on themselves." (90:47, Marc)
• Personal Toll: The emotional cost of Jill’s death nearly broke Marc physically and emotionally; he finds renewed resolve in his responsibility to his children.
• Hope for Breakthroughs: Gene reprogramming initially developed for Jill may extend to reversing non-inherited (epigenetic) forms of autism, and potentially other disorders (Parkinson’s, Alzheimer’s, rare genetic conditions).
• Multi-Pronged Strategy:
  1. Gene Reprogramming: Targeted to restore expression in silenced or mutated genetic material.
  2. Cancer Stem Cell Drug: Move rapidly into patient trials for broad-spectrum anti-cancer adjunct.
  3. Direct-to-Consumer Inflammation Therapy: Nutraceutical stack for rapid global impact on milder neurodevelopmental or inflammatory disorders, engineered to be safe and widely accessible.

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Philosophical, Technical, & Practical Insights

• On the Nature of Biology:
  • “Biology can only be solved if we change the conditions, not just go in and break something and fix it.” (34:19, Marc)
• On the Human Spirit:
  • “The science might not be the most important part… it might actually just be a story of how far human will can push.” (127:46, Marc)
• On Systemic Health Decline:
  • "If we're not successful here, two, three decades from now, the human race is going to start going off a cliff… If we don't have our biology intact, we don't have anything." (131:04, Marc)

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Notable Quotes & Memorable Moments

• On Grief & Resilience:
  • “The only way out was through… what you need most is where you least want to look.” (79:51, Marc, referencing Carl Jung)
• On Medical Breakthrough:
  • “No gene or receptor had ever been switched back on in a living human before, let alone two across chromosomes.” (26:55, Marc)
• Practical Wisdom:
  • “I never ever believe that things can’t get better or go away… But I often tell people, even though miracles do happen, we can’t standardize miracles. All I have the power to do is do something that I know can work consistently and reproduce over time.” (118:44, Marc)

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Key Timestamps

• Marc’s Early Life & Hardship: 03:12–10:39
• Jill’s Diagnosis & Immediate Response: 11:57–18:34
• Gene Reprogramming & Receptor Reactivation: 22:58–39:13
• Breakdown of ‘Triune’ Therapy: 22:58–27:18
• Philosophy of Science & Biology: 34:19
• Cancer Stem Cell Elimination: 54:45–66:01
• Challenges with Medical Establishment & Funding: 68:41–76:13
• Aaron’s Collapsing Genome & Marc’s Next Mission: 77:37–100:33
• Three-Track Master Plan (Gene, Cancer, Consumer Product): 100:33–105:30
• Inflammation, Diet, & Broader Health Discussion: 112:52–117:25
• Scientific Philosophy & Closing Reflections: 120:04–132:42

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How to Support/Follow Marc Malone

• Twitter/X: @realMarcMalone
• Website: ahmedbiogenetics.com
• Upcoming: Decentralized science/token project for direct-to-consumer therapeutics.

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Final Reflection

This episode blends heart-wrenching tragedy with scientific audacity, showing how desperation and love can drive innovation where the system fails. Malone’s paradigm-shifting insights into gene reprogramming may herald a new era in treatable disease, but his greatest message is the indomitable will of the human spirit—“Half the world is sick and the other half are the family and friends of the sick.” (00:58, Marc, echoed at 127:46 and 132:02)

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Transcript

[A]

All cancer uses these pathways to generate if we are able to cut the regenerative engine at the root. This truly is the closest to a cancer cure proven in a human that we've ever had. So the cancer she had is called triple negative breast cancer. Less than 1% with her cancer would survive three months. Part of the thing was, number one, getting the right molecule that could crack the cancer open. Number two was to starve its energy. And then the third part was intracellular signaling, which is what made it work in a human being. And the halved in a week in like the most ultra aggressive, lethal treatment resistant possible cancer case. This gene reprogramming that I was able to do, which many see as one of the greatest scientific advances of all time, was just removing things that were suppressing biology. If we succeed, we're going to be able to essentially restore even the worst of genetic disease mutations. This is something that affects every single person on earth. Half the world is sick and the other half are the family and friends of the sick.

[B]

All right, good. Well, Mark Malone, I've been looking forward to talking to you, man. I appreciate you flying into town to chat with me today. You're working on some big stuff, man. And I think that cancer has got to be one of the biggest, most important topics that we could be talking about about. So that's not everything that you're working on and doing, but it's, it's, it's a big part of it. And if what you're doing is, has a chance to help people, then this is a big deal. This is a big conversation. So why don't you just go ahead, introduce yourself and tell us a little bit. Maybe tell us a little bit about your story as well and then we'll take it from there.

[A]

Yeah. Thanks for having me on, Matt. This is a cool setup you guys have got here. Yeah, I love it. It's awesome.

[B]

I appreciate it.

[A]

We have an alien looking at me as I have to talk about curing cancer. So that's, that's something, you know. So an interesting thing about this is, you know, I didn't have any scientific background. Now I actually did study for a little bit online at Oxford philosophy of science, but it wasn't like a full degree program. I got some understanding of how scientific mechanisms work, but I'm basically completely self taught. So I guess I could start right at the beginning because maybe it makes sense if I start right at the beginning. I also want to start right at the beginning because when it comes to my wife and my Son, if you don't. If that was the only hardship I had faced, you could understand when I would say it's like the worst possible thing. But actually, I've experienced hardship my whole life, and I can tell you that in contrast to the other hardship, what happened with my wife and what's going to happen with my son if I don't succeed is indeed the worst possible thing. So I was born Coventry, England. My father had pretty severe mental illness, was institutionalized a couple of times. My mother had chronic sickness. She had autoimmune disease. She was bedridden for most of my childhood.

[B]

What was your dad's. What was your dad's condition?

[A]

He had like a. Basically a severe major depression with some bipolar, but it was mostly just severe major depression. And, and, and he actually voluntarily, by the way, institutionalized himself. He chose to do that for, for to try to get better. That was when I was a baby. So we were surrounded, we were in pretty severe poverty. We lived in what's called a council estate in England, which is kind of like government housing, welfare. There was five children and we were surviving on probably the equivalent of about 250 a week. So there was. I was surrounded by drugs, I was surrounded by violence. There is a childhood experience test called the ACE score. Adverse childhood experience. I have 10 of 10 every single childhood trauma.

[B]

I think my wife has nine out of 10.

[A]

That's intense. Yeah, yeah, it's extreme.

[B]

Yep, yep.

[A]

So everything from like family members going to prison, suicide attempts, overdoses, drugs, poverty, violence, sort of abuse, neglect. And you know, the thing is when, when I say that, because I want to point out something important, which is one, just because you were born into an environment like that doesn't mean it has to define what you become.

[B]

Right.

[A]

The other thing is, though, when I explained what happened to Jill and what happened to us and, and how extreme and how hard it was, I just wanted to know, in contrast, that it's not like I didn't know what hardship was already. So the point is, is that that was kind of the background. And one of the hardest things about the background was when I was younger, a few people saw that they would call me gifted in quotation marks. I say that because I don't really know what that means. Maybe everyone's gifted, but they, they said I was gifted. But the school system never really ever gave me a shot. They didn't, they didn't take me seriously because I didn't show up for school on time because I didn't have clean clothes. I Used to have to scrub my school sweater with a sponge under the sink. We didn't even have money for washing detergent sometimes. And my mother was sick when I was 10, so I'm like, scrubbing my school uniform under the sink. And the school system didn't take me seriously because they were like, well, he's from some drug den. You know, he's not with. You know, he's a lost cause. But I was always deeply interested in how the world works and how things work, whether it's on a spiritual front, a philosophical front, or a scientific front. Ever. Ever since I was super young. And when I used to do those sort of, like, exams in school, I would get almost 100. And even though I'd get like a hundred percent, they still didn't put me through to any top class or. Or anything. So I gave up on it because they gave up on me. They never gave me a chance. So I was like, wow, the establishment, the school system, education, it's. It's not a place for me. So I completely sort of abandoned it. And then I went through. I lost my brother when I was 20. Missing persons. Wow. And Aaron. My son is Aaron, named after Uncle Aaron. And Aaron was the most important person in my life. He was. You would have liked him, and he would have liked you because he was deeply into this consciousness. He was deeply into the way that the higher reality worked. And thank God for Aaron, because Aaron was the one person that believed in me truly and got me through that sort of childhood process. And then what happened was he went missing and July 2012 and has never been seen since. His wallet, his phone, his passport, everything was in his house. He didn't run because he didn't have anything with him. He's just gone. Missing persons is a hard thing to do with because it doesn't come with any closure.

[B]

Right.

[A]

So I kind of. So I was a musician in my early 20s. I loved music. I still wish I could be a musician, by the way. I. I love music. Unfortunately, I've been pushed to curing cancer, but I. One day I hope to go back to be a musician. And I was a musician in my early 20s. And then I was sort of going off the rails because it was. It was. I hadn't. Aaron had gone, and I didn't have that person to sort of like, believe in me. And then I met Jill. My wife was interesting as she came up as a people you may know friend request or a friend suggestion on Facebook. So she came up and I saw her picture and I was like, man, that is the most beautiful thing I have ever seen. I was just captivated by just how beautiful she was. And then so I added her and we started talking and I couldn't believe it because she was so intelligent. She was so. She was deeply spiritual by the way. She would, she would do juice cleanses, she had crystals and she had sage and she had. And she also had bibles. And I was just, I just can't believe it. The most beautiful woman I've ever seen and also the one that actually understands my idiosyncrasies in what I believe. So we started talking. We hit it off straight away and within six weeks of us talking, like on Skype, back in those days when there was a Skype, this was about 10 years ago, she came to visit me in England. And the day I met her, I told her at the end of that day that this has been the greatest day of my life. And she said, mine too. We got engaged 10 days later. I moved to America four months later. And then we got married a year after that once all of the immigration process and stuff had done. So what had happened is when I met Jill, she I guess gave me the anchoring to dig deeper and like know I'm better than what I was becoming because I. I wouldn't have been able to do any of this stuff without her. So we got married in Santa Barbara, November 17, 2018. And then we had our children. Aaron, my son, who we'll talk about today for sure was, was born on March 12, 2020, when the world was shutting down. And that was an experience because I came out of the hospital with this baby and in a Southern California too, where it's super like, you know, busy, a lot of people and it was like Close Encounters of the Third Kind. There's like no one there. And I was like, this is crazy. Like of all imagine like coming out in LA and just seeing a dead zone. It's the freakiest thing. Well, I was like, what did I bring this child into?

[B]

Right. My son was born in April of 2020, so.

[A]

Oh, right, yeah.

[B]

So coveted baby.

[A]

Yeah, yeah.

[B]

The only two people out in the hospital, my wife and I, you know, in the, in the room, right? Yeah, yeah, Crazy, crazy.

[A]

It was. It insane time to have a child. But you know, we didn't know that was going to happen though I still had another one, even though knowing it was happening. Cuz then my daughter was born a year later, Iona. So we had three children.

[B]

And my birthday is one day away from your anniversary is it? Yep. 18th, 17th, 16th is my birthday.

[A]

So we met in Southern California, got married there, Aaron was born there. And then we, we moved to Arizona and then we moved to South Dakota and we kept kind of moving east towards where the freedom was because during COVID times places were very restrictive. My wife was from Minnesota originally, so we were basically moving close to Minnesota, but we ended up in South Dakota. Everything was like totally open the whole time, but we were close to her family, so that's kind of how, that's kind of how that happened and how we met. And then in the late, late January 2023 she got diagnosed with the cancer. And it wasn't just any cancer, unfortunately. So the cancer she had is called triple negative breast cancer, which already is one of the more aggressive cancers. But on her side she had a bunch of super rare mutations underpinning that, which we can talk a little bit about, but basically making it like the, an ultra lethal, ultra treatment resistant aggressive cancer. For context, less than 1% with her cancer would survive three months. Even pancreatic cancer, 20% survive a year.

[B]

Yeah.

[A]

So you're looking even conservatively 10 times more lethal than the worst form of cancer.

[B]

Wow.

[A]

And I can explain all of the specifics of why that is, but needless to say, you're talking maximal aggression, maximal treatment resistance, already metastatic upon diagnosis. And it was, it was crazy because I was just kind of like, I knew looking into it very early. We spoke to some doctors, I looked at the. This was pre AI. There was really no GPT or Google AI. I think GPT had just come out, but everything was still just normal Google search. And I was looking through the papers, I was looking through PubMed, NCBI and I realized the prognosis, like conventional treatments and frankly even most alternative treatments just had absolutely no chance. Yeah. Of working. So much so that they, with her specific type of cancer, they even removed her from clinical trials like because there was no response. So they were like this group, we're basically going to exclude them from the clinical trial results. So by any metric there was just nothing that could be done. And that's why I had to do something. And I guess that's brings us to why I had to face down pretty much the most lethal form of human disease possible.

[B]

Wow, that's incredible. That's incredible. And so you guys, you were living where, where were you guys? You, you moved to the US and where were you living?

[A]

Yeah, so when I first moved to the U.S. we're in California.

[B]

Okay.

[A]

That's why we Got married, and Aaron was born, and then we moved to Arizona and South Dakota. So when this started, it was in South Dakota.

[B]

Okay. And so what's going through your mind as you get this diagnosis? And you guys are talking about it and you're thinking through this. Are you thinking at that point, I've got to do something about this because the doctors are not going to do anything? I mean, when did that kind of enter into your mind, that I've got to be the one to take charge here?

[A]

Yeah. Straight away.

[B]

Yeah.

[A]

Literally the first day, which is absolutely insane, and I don't recommend anyone else do this, but I knew I had to. And I knew, like, instinctively that I could. Can't explain that part because it makes no sense, because we are talking about pretty much the most lethal form of human disease here. But I knew I could, and I looked. And the reason that I knew I had to is because I just knew there was no shot anywhere. Any anywhere. I knew we didn't have a shot anywhere else. So in my mind at the time, I had to kind of suppress the. The. The anticipatory grief, the.

[B]

The.

[A]

The pain that wanted to come up. The part of me that just simultaneously wanted to break down and also wanted to just break everything else, and I had to kind of switch into war. You know, and the reality is, is every day she was going through that disease, and to some degree, every day now with my son, I am in a war, and I don't. I don't have the luxury of breaking down.

[B]

Right.

[A]

You know, so when she. Later in the story, you know, when she passed, and we'll get there then. Then it broke me pretty hard. And that's. That was a necessary, natural part of the journey.

[B]

Yeah.

[A]

You know, but at that time, when it. When there's a fight, when there is a water fight, I'll fight it, and then I'll cry later, which is. You know, it's interesting, actually, because I had a friend of a veteran who told me the guys who come back from war with the worst PTSD are the ones that don't cry after the battlefield.

[B]

Right.

[A]

Yeah.

[B]

Right.

[A]

He was like, the ones that cry after a really rough day, they've seen a really rough thing. They always come back healthy. It's the ones that bottle it all up.

[B]

Right? Yeah. It's called. If you. It's called Relive to Relieve. I just did a podcast on this.

[A]

Oh, really?

[B]

Yeah. It actually moves the traumatic incident from one part of your brain to a different part of your brain. If you go Back to that incident. Usually, you know, PTSD is from childh. And so you imagine yourself as a child and you relive the event. You go, you don't, you know, analyze it, you don't judge it, you just, you're just there, you're just in it again and you watch it happen. And that, that if you do that four or five times, it, it, you still have the memory, of course, but it makes it much less. It's not, it doesn't have a hold on you, it doesn't have a grip on you. You don't get triggered by things in your day to day life because of it, you know, and it's. Yeah, it's very, very powerful.

[A]

But so I need some of that.

[B]

Yeah, yeah, it's, it's a super. It's like the only thing that works for. I mean, there's a couple of things that work for ptsd, but, but anyway, so what did you, what did you do then? What were your first steps in order to try and, you know, do what you could to, to help the situation?

[A]

Yeah. So, and this is kind of a difference of how my brain works to conventional scientists or perhaps to a lot of different types of people. But when I first looked at her disease and I was like, okay, again, we're doing the analog, we're not able to speed things up with AI. We have to look through Google, Google Scholar papers, PubMed. And I'm looking through and I'm like, there's not really any simple way to crack this disease. So what I did is I had to start drawing out and I literally drew it out. It's like I need to draw out a causal pathway. See, most scientists think of things consequentially and not causally. So most scientists, and this is a philosophy of science problem that most sciences think, okay, A goes to B goes to C. Right. And they go, okay, so if we can sort of pause B, we won't get equal C. Whereas I think if I can remove A, then there is no B and C. If I can find a way to figure out what is actually generating this to begin with, what is causing this disease to take over the body at the deepest molecular level. And if I can get to that, we have a chance. Because I was like, there's no way of reactively fighting this. Because we're talking a cancer where tumors are growing 1 to 2 centimeters a week.

[B]

Wow.

[A]

For contrast, typical breast cancer grows 1.7 centimeters, I think, every 18 months.

[B]

Yeah. Wow.

[A]

So like 75 times the speed. Right. So there's no way of reactively winning. Even if we had a super successful reactive treatment, like some kind of antiva type thing, like some kind of specialized immunotherapy or some specialized MRNA MRNA therapy, or even some specialized chemotherapy. The reality is there's no way to reactively beat something that is this fast and that is this treatment resistant by nature. So I had to diagram out what is the deepest level that I can get to. Because if I can close the door from these cells being created, we have a chance. But I got to find a way to close the door from this thing being generated and then we have a shot of doing it. So that was kind of the goal from day one for the whole year. It took me some months to figure out how to do that part. That was much later, but at the beginning that was still the goal. I didn't manage it, but I managed, I did manage something perhaps even more advanced. So then I had to find compounds. I was like, okay, how can I crack this treatment resistant shell? So let me give you a little more of that detail I didn't give earlier. There is a known. One of the most common cancer protective genes is called TP53. Okay. That's a gene that basically protects you against cancer when it's mutated. It doesn't protect you against the cancer. So then people with a mutated TP53 often get cancer more than people without it. Her TP53 was not just mutated, it was, it was gone. Which meant there wasn't just a broken protection mechanism. There was no protection mechanism. So it was just all out war in the cells. Then she had these things called mismatch repair genesis. And these are going to be relevant for Aaron. They repair broken DNA. So inside of us, when we get sicknesses, when we get exposed to toxins, when we get exposed to pathogens, our DNA can break. And these genes repair that DNA inside of you. So the job of a DNA repair gene, especially in a cancer context, is to repair the DNA so it doesn't become what we call oncogenic cancer. Jill had a broken mismatch repair gene too, actually. So that meant that the DNA repair wasn't working either. So you had no guardian to stop it, the cancer. Then you had no DNA repair underneath it. And then you had a super high aggressive rate. So it was pretty much like the most hostile cellular territory. But what I discovered is I need, if I could, the triple negative. Breast cancer is characterized by silenced genes. What if you imagine a cell like, imagine like a circle and on top of a cell you have things called receptors. And receptors like they, they take in your hormones, they take in your insulin, they take in all of your energy. Every cell has a bunch of receptors, things on the top like antenna, like taking in a signal necessary for the body to work, especially in things like energy, hormones, etc. So in her cancer receptors are silenced, they're switched off. Hormonal genes don't work, so she's not getting any estrogen, progesterone, etc, so the, the, the receptors are switched off. By definition, that's what this disease is. Triple negative breast cancer means estrogen, progesterone and HER2 receptors are switched off. So that meant her hormonal receptors at the top of the cell are not taking in hormones, they're off. That massively speeds up this aggression because. Yeah, there you go. And that massively speeds up the aggression because they operate as somewhat like protective genes to like slow the cancer down. That's why in typical breast cancer where you have hormonal involvement, it's way less aggressive than triple negative breast cancer. So those genes were switched off. Now what I was trying to do was find a way to crack into that tumor. And what I ended up doing as, as a journey on this byproduct was actually switching those receptors back on. So I found something in the streptomyc's family which is used for antibiotics, which is used for anti parasitics.

[B]

What is that? What is that?

[A]

Streptomyces. So that's the, that's the plant, the molecule that creates things like ivermectins, that creates antibiotics. So it's used for a lot of different anti parasitics and antibiotics. So in this case what I used was a streptomyc's avermectins, which is, it was a sister and a form of like the ivermectin. But the difference with what we did, we had to re engineer some of this in the pharmacy. So I got the doctor and the pharmacist to re engineer some of this to make it work, meaning that we had to improve its delivery system, et cetera. So part of the thing was, number one, getting the right molecule that could crack the cancer open. Number two was to starve its energy because cancer like this, all cancer, but especially super aggressive ones like this are driven by, I'm trying, I'm trying to not go too complex. Driven by glycolysis and glutaminolysis. So in other words, glutamine and glucose, more than oxygen are used as the Cell's energy. So what we call aerobic glycolysis is basically the cell is using glucose even when oxygen is present. It what it does, it does that to make it more efficient. It does that because then it can replicate faster and go throughout the body. Okay. So the second part was to starve the cell of that energy so the cancer cells couldn't keep replicating, couldn't keep pulling in that energy to become treatment resistant. And then the third part was intracellular signaling. So if you imagine inside a cell, we talked about the receptors at the top inside the cell, you imagine it like you have a network, like a train track inside the cell. You've got all these different train tracks that go to different places. And if you go across one track, the cell will live. If you go across another track, the cell will die. But I found a third track which was the cell transformed. It didn't die, and it also didn't live. It transformed. Which again, wasn't really thought of to be possible. So what this meant was we had the energy part, we had the compound that could crack open the hard locked genes that were locking down those receptors. And then the third part was this intracellular signaling, which we call signal pathways. And I triggered it where it transformed the cell and those receptors and genes came back on. So not the amazing thing about this is one, no gene or receptor had ever been switched back on in a living human before, let alone two across chromosomes. Because inside the human body, we have separate chromosomes that carry maybe 100, 200 different genes. So in this case, you have chromosome 6 that has oestrogen and chromosome 11 that has progesterone. These are completely different chromosome areas holding the gene, which sets a very different precedent to what gene therapies and MRNA have been doing. Because that meant that we triggered receptors and genes back on in completely different chromosomes in completely different areas of the body. So because of this, we never had a gene reactivation in a living human before. Certainly never two, certainly never across chromosomes. But perhaps like, from an ontological standpoint, what I mean by ontological is like, from, from a perspective of the purpose of disease, we actually reversed the purpose of the disease. You know, it's like, it's different to just curing a disease. It's like actively reversing it. Because the nature of this disease is to have those things switched off, so to switch them back on and then watch the tumor shrink. In many ways, I think it's actually the first instance we've seen of cancer actively reversing, not just being Killed, but reversing, because, like, the purpose of this cancer is to have those genes off. They came back on, and then the tumor started to shrink. In fact, we saw one of her metastatic tumors disappear completely. And the primary best one went down 70 to 77%.

[B]

Wow.

[A]

So it was like watching an active ontological reversal, like watching an actual reversal of the nature of the disease, not just watching the disease die. So what we'd done is we transformed it by hitting these receptors back on. By the way, it has unbelievable ramifications because of course, estrogen, progesterone are necessary for human life procreation. I mean, we have 1 or 2 billion, who knows how many. But anything from 1 to 2 billion infertile people in the world, environmental exposures, you know, plastics, toxins, numbers increasing all the time. And it's going to be way higher in the younger generation who are exposed to this in utero. And then as they've come out.

[B]

Right.

[A]

So the key to reversing a lot of those problems is exactly this, is to have the hormonal genes switched back on and working.

[B]

So they were completely off. They were at like 0%.

[A]

Undetectable.

[B]

Undetectable. And then did they come back to full strength or did they come somewhere in between full and sleeping?

[A]

Yeah, So I probably should have mentioned that. Of course, when I was doing this, this was all physician oversight. Her disease was diagnosed by biopsy. Right. So biopsy obviously said, okay, no estrogen or progesterone genes or HER2 in this tissue. They are undetectable levels. We had the biopsy from the hospital, signed by the physician and surgeon, etc. Then I did this treatment. Three weeks later, we did another biopsy. This was a blood draw called a liquid biopsy. And the liquid biopsy basically detects shed tumor cells throughout the blood. So rather than pulling like the tissue from the tumor directly, it detects all of the tumor cells throughout the blood that are coming off the tumor that's spreading throughout the body. And then it analyzes the tumor cells through the blood. Okay. So a liquid biopsy is very common in standard oncological care because you can't do tissue, tissue biopsies every week. Right. It's. You would traumatize the patient. It's too expensive. And of course, you could cause the cancer to get worse. So liquid biopsies are standard of care procedure. And what they do is they monitor where the cancer is in the blood. So three weeks after we did the initial biopsy, we got the liquid biopsy, which showed estrogen and project Progesterone had come back on, so 15 progesterone and 25 estrogen, which was equivalent to what most of the other genes were expressing, you know, in, in the biopsy. So when we look at the panel, I have the panel in the paper, but when you look at the whole panel of other genes, it's equivalent to. Because the genes are never like 100 expression, really, because they are, they're especially in tumor tissue. So, yeah, basically that's a two and a half thousand percent increase, like from undetectable to 25. And what's interesting is even if we were to look at the fact that one is tissue and one is liquid, if there's some like, measuring discrepancy, because there will be some measuring discrepancy between a physical and a blood one, the measuring discrepancy would be at like at most 100. So 1 or 2%, not 2 and a half thousand percent or 25%. Right. So maybe if we'd done it from the tissue, it would have been 20 expression, not 25 is what I'm trying to, trying to say. But the, the, the discrepancy between liquid and physical is nowhere near 25 times the difference is what I'm saying. So even if the expression difference was, there was a discrepancy there, it really wouldn't have changed the outcome at all. Yeah, the outcome is still the same. I remember when the doctor read that to us and he was like, you do have Eastern and progesterone genes. And then Joe was like, so confused. She was like, what? And I was like, I knew that was going to happen because I was reading in the paper when I put together this treatment that there was a, these locks I was unbreaking syn3h. DAC could switch those receptors back on. But we, I didn't know it was actually possible in a human, this was in a mouse, but I did know it could have happened and it actually happened. So if you think about like a chromosome, like you've got these layers, these layers like, of, of coating. It's like literally think of it like clothing and the layer on top of a chromosome, it's like holding all the genes and protecting them and holding them in place. That's like this syn3 part. That's basically a part that is holding genes in place across thousands of genes in the genome. And then underneath that you had this hstack part and that's locks underneath the material. So it's like having another layer underneath the clothes. And those layers are to protect the genes because we need them protected, because we're exposed to viruses and bacteria and toxins. So it's a. It's a natural part of biology of the genome for these genes to be protected. Of course, but in cases like many diseases, and not just this, a billion or more people's diseases, neurodegeneration, some Parkinson's, some Alzheimer's, some autism, those genes are switched off. It's no longer protective. The control system has tightened them too much and they don't work. But for the other 7 billion people, that. That layer is protective, but for some, it's enforcing too much protection. So what we did is we opened that back up and yeah, I mean, it was. I knew some parts of it had been done pre clinically, but they'd never been able to figure out how to do anything like this in a human. And the reason that I was is because they only had one piece. They had that synth re HDAC piece, but there was a metabolic piece and there was an intracellular signaling piece that I built with it, which is what made it work in a human being. So, and the thing is, with most science goes back to most conventional scientists, they view the genome, they view humans kind of like. Like we're like a machine. So they think, okay, if we just go in and break the gene and edit it, the person's going to be fixed. And that can happen sometimes. But biology, like, the genes aren't like, isolated. They're part of a communication system. Like, your metabolism is communicating to these genes and your hormones are communicating to these genes. And. And it's just like everything within the biology is actually connected and aware of everything else. And the problem is, is when we look at humans like, like a neutral machine, we're gonna miss the point, right? That's not how this works.

[B]

Screw, and everything will be fine.

[A]

That's right, but it's not how it works because of course, everything is connected to everything else. Blood flow is connected to insulin, which is connected to hormones, which is connected to sleep, which is connected to stress, which is connected to glyphosate. And everything here is in an interconnected web. So the reason I was able to do this gene reprogramming was because I realized that biology can only be solved if we change the conditions, not just go in and break something and fix it. Instead, I changed the cellular conditions with different molecules and targets to allow the genome to re express itself. Like, all I did is remove locks, you know, So I, when I went through that whole thing, the syn 3h stack the metabolism. Just think of it as all I'm doing is removing blocks, I'm removing locks, I'm removing metabolic pressure, but all I did is remove stuff. The genome itself is what restored itself. I just removed the blocks. It is a little bit like the Constitution. I know that might sound like a weird segue, but I promise it's going somewhere. So if you think about the, the Constitution, why it works so well, it's via negativa. So our law and English common law too. English common law, the American legal system, but the Constitution really enshrined that common law. That's why it's better. But it's a via negativa process. So the way it works is rather than like European Union law, which is why I voted to leave the European Union. EU law compels you to do something. It says you must do X, Y or Z. Whereas English common law, particularly in constitutional form, doesn't compel you to do something. It says what you can't do and then everything else you can choose to do for yourself. So it says you can't invade someone's privacy, you can't take someone's property, you can't take someone's right to self defense or their right to speech or belief, but as long as you don't take those things from people, you can do whatever you want. That's completely different methodology to saying you must do XYZ for society to function. Instead it's like, just don't do these 10 things in the Bill of Rights. Just don't take these 10 things from people and society will function fine. And honestly, this is a micro macro thing. It works at every level of reality the same way. This gene reprogramming that I was able to do, which many see as one of the greatest scientific advances of all time, was just removing things that were suppressing biology. It was the same approach as what we do in our legal system. It was to say if we just remove the things that are oppressing us, life takes care of itself. Life expresses itself correctly.

[B]

It balances.

[A]

Yeah, yeah. So it's really, and I, I, I, I see it in every area of life. The, the pattern is the same. Rather than trying to compel reality to conform to what I think, it's better to just try to remove the things that are suppressing us. And life takes care of itself in the same way. It's like the difference between philosophy and ideology is that ideology is like me trying to bend reality to my will and philosophy is you trying to bend your Will towards reality, you know, And I think the goal of good scientists and philosophers and thinkers and humans is how can we best match reality with the right intention rather than trying to bend reality towards us. So that's largely how we did that. And then that happened in the first month. And things were looking really good because the tumors were going down rapidly. And she was in awesome health. She was getting better. The problem is I couldn't sustain the gene reprogramming. And the reason I couldn't sustain it is because back then, this was three and a half years ago, I didn't know how to get that metabolic starvation just in cancer cells. So I couldn't maintain it because I was starving her too. So after a month of doing it, I couldn't do it anymore because I was like. Any way I. Whether it's fasting, whether it's a drug or a molecule, there's no way to separate the starvation from her and the tumors.

[B]

Right.

[A]

Now, I have figured this out since, but it took me three years. I just started it back then. So I didn't have the answer for that back then. So without that metabolic part of what I called the triune system, those three things, the gene reprogramming couldn't sustain, which meant I couldn't sustain the cancer reversal. Also couldn't sustain the receptors being back on.

[B]

So.

[A]

So we had the proof of concept. We had the tumors eradicated, we had the genes back on, but after that point, she started to decline again because I couldn't sustain it. I didn't know how to starve. Isolated tissue in the body, which is what cancer is, right? It's like isolated tissue. I didn't know how to do it without starving her. So after a month, the cancer started rapidly growing again.

[B]

Okay, yeah. Let me ask a question first before we continue on, on, on this track. What, this all happened within a month of the diagnosis, Is that right?

[A]

The gene reprogramming happened in the first month.

[B]

So, so what, what was your prior knowledge to genetics and all this medical stuff you know, coming into this? I mean, you're self taught, obviously, right?

[A]

Yeah.

[B]

So when did you begin? When did you start to learn enough to be able to even have enough, you know, information and intelligence to be able to go down this path?

[A]

So I guess I did do some very deep dives into biology the. The three years prior when Covid started.

[B]

Okay.

[A]

But not cancer. So I did start to understand. I spent a couple of years deeply understanding some biology, but I didn't really understand cancer. And then I had to Apply some of that baseline understanding to cancer when this happened. The truth is, is that the vast majority of this understanding came exactly as it was happening at the time. Yeah.

[B]

Wow.

[A]

Yeah.

[B]

So you're a fast learner.

[A]

Yeah, yeah, yeah, yeah. I. I know. I. You know, I have had to be. I've had to be. You know, it's kind of a. It's an interesting thing, though, because I tell you, there's something else going on here, and this isn't me coming out like, as, like a cult leader and, and saying that I'm like, spiritually divine and you should follow me or anything like that.

[B]

Everyone's spiritually divine.

[A]

Right? But there. What I mean by something else going on is that there was an instinct put in me. Man, the academics are going to take this and say I'm insane, But there was an instinct on that first day that was put in me that gave me the first step of where I needed to go.

[B]

Nice, nice.

[A]

You know, so this metabolic thing is a prime example.

[B]

What was the instinct? What. What did that feel like?

[A]

It literally, I sat down at my computer, I realized how bad the situation was. I realized no treatments were going to work for her. And then based on that earlier viral research I did and all the biology for the prior years, I remember thinking, oh, there was a viral protein replication inhibitor to deoxyglucose, which worked for. Which, by the way, I discovered for Covid back in April 2020. And then the Indian government and all the big science journals figured it out 18 months later to the oxygluc. Basically, it hijacks the viral replication system and breaks it down. It's like a fake glucose mimic that goes into the system and then the viral attaches to it as an energy source, but it's not real, so it breaks the virus down. So it's a really clever way because viruses like cancer hijack our metabolism. But cancer is way worse because it's got the whole of human evolution behind it. A virus is a dead entity, but cancer is living and has the intelligence of. Of human cells. Anyway, I digress. So that instinct was tied to three years earlier when I started looking at Covid, where I was like, viral protein replication inhibitor. I remember two deoxyglucose that I discovered to start using for Covid back in April 2020 also had some use in cancer. So that was the first moment I remembered. Oh, okay, so then if I can find something. So then I was like, so what's the most effective protein replication inhibitor in viruses? Maybe that will work for Cancer. And that's what brought me to the streptomyces family. These ivermectins, these antibiotics. And then from there I looked at the cancer papers and I was like, yeah, this is it. These actually can. So it was like a chain of thought like that. And that all happened in the space of a couple of hours and. But the metabolic part was just like, given to me. Professor Thomas Seyfried from Boston College, he's done a lot of deep work on cancer as a mitochondrial disease. Now, he's not correct fully that it's a mitochondrial disease, but he's correct that it is largely a metabolic disease, but it is also a genetic disease. Again, everything's intercommunicating. It's not one or the other, it's the whole system. But I love his work. I appreciate him a lot. He. His video came up on YouTube the day of diagnosis and taught me that cancer was driven by glutamine and glucose. Like the day of the scan, had that not happened, this triune system would never have happened because this metabolic part was one third of that system.

[B]

Right, right.

[A]

Well, so some of it was like serendipity, some of it was building off prior knowledge. But there was a lot of things that had to come together super fast for this to work. And it was a bit like a download, you know, there was a bit of a download there. Now with the functional cancer cure part, where we eliminated the cancer stem cell pathways later in Jill's journey, and that's actually much more closer to a cancer cure than this. That was not. That was fully me, but the gene reprogramming was like partly just dropped in. Parts of it were dropped in my lap, you know, so that was the first month, but I couldn't sustain it. So then she started getting sicker again. We tried a bunch of things. We did. She. We did surgeries, we did immunotherapy. None of it was working. And Jo was a good candidate for immunotherapy. She had PD L1 expression, which meant it should work, didn't it literally did nothing. Like, literally nothing. Didn't even buy a day. So she started to decline. She had this surgery on the breast. They took the tumor. The cancer was so aggressive that the tumors all grew back within a couple of weeks. Like five tumors where the breast used to be. Because she was losing so much weight, they couldn't skin graft. So I had to clean her wounds with these open tumors on her rib cage.

[B]

Wow.

[A]

Every day, Joe was like my height, like 5, 10 and she was so. She was a tall woman and she was dropping down to like 80 pounds. The cancer, the cachexia was like sucking away all of the nutrients in the life force. So they couldn't do a skin graft. So where they used to have the tumor, she had all these, like, little tumors popping up. And she had five of them there on the breast. And I used to clean it with saline and put bandages on her every day, and she would scream in pain. I used to administer a morphine and.

[B]

Yeah, sorry, take your time. That's tough.

[A]

Yeah. So the children were 0, 1 and 3, And she was rapidly declining. I couldn't. And at this point, I couldn't even do the gene reprogramming again because she was. I mean, I would have starved her before I starved the cancer. It would have just killed her faster. And I didn't know how to make this more targeted back then. And I failed.

[B]

But.

[A]

I had to do the wound cleaning, take care of the babies. They were babies then. I've raised them myself now. But we had some support came in so I could focus back on the research. There was a. There was a couple of months there where I had to just be like, full caregiving of. Of her and the children. And then we went to Arizona to try to do some genetically targeted chemotherapies and immunotherapies and a bunch of natural treatments, IVs, like things that have good clinical efficacy. There's a lot of natural treatments that have clinical efficacy. The problem isn't the natural. So this is where conventional scientists and naturopath type people talk over each other because they're both looking at different parts of the same picture. A lot of the naturopath types will say, look, there's this study, I've got papers here with resveratrol for cancer. Resveratrol is an amazing molecule to fight cancer. The problem isn't. So then a conventional scientist will say, there's no human proof of that. It's all like labs and it's all just like anecdotes. The reason that the resveratrol doesn't work when we apply it to mass cancer cases is because of bioavailability. The problem is that natural molecules, they do work, but only about 3% of it actually reaches the cancer. That's the problem. We're not able to. At least we weren't until I started doing this work. But I've figured it out largely how to do this, how to transport these powerful molecules to where the disease actually is, because that's really the biggest stumbling block. So you have two people where the oncologist is correct that if you try to just do resveratrol, IVs or curcumin or whatever for, like, all of these struggling cancer patients, there's a chance that it's not going to work for most of them. But the person who. Who sees why it could work, the naturopath, they see they're seeing something. Clearly what they're seeing is true. It's just those two systems never came together to figure out how to actually take those molecules and make them effective agents. That's the problem, because I saw this in Jill's case, too. We did a lot of natural IV treatments with her genetically targeted chemotherapy. So they took chemotherapy specifically that matched her tumor markers. Couldn't have been more precise. Not only did it not help her, her cancer grew faster during that treatment. We did everything. We did hundreds of treatments. I'm talking every repurposed drug. Fenbendazole, mebendazole, metform, every iv, vitamin C, resveratrol, curcumin, chemotherapies, many different types, immunotherapies, surgeries. Jill got worse through all of it. Her cancer was unstoppable. It just blasted through all of it. We had the weekly biopsies throughout treatment. I've got all the records, of course, and some of them are in the paper. And you can see the mutations just growing and getting angrier through the treatment. You know, like it's an upward trajectory.

[B]

How do you mean? What is that?

[A]

So in those liquid biopsies, they. They sequence for specific, like, mutations, like tumor mutations, and we see if they're going up in the blood or going down. Okay, Right, Right. So it's. It's called a vaf, an LL fraction. So what we do is allow frequency. So what we do is we see is this gene going up or down because that kind of indicates to us whether the treatment is working. And through all of Jill's treatments, aside from the triune gene reprogramming right at the beginning, up until this point where we'd done all of these treatments, her tumors were growing every week. So cancer was proliferating more. Basically, it was getting through more of the body, more of the blood, more organs, and even right to the tumor mutations themselves. They were just getting stronger. Yeah. So we were now at the place where it was, like, very obvious that she was going to die soon.

[B]

And how far along after the diagnosis?

[A]

Yeah. So at this point, it was this. By now, we're at August 2023. So it'd been eight months.

[B]

Eight months. And what was the original estimate from the doctors?

[A]

Well, the, and basically, with her type of cancer, she should have been dead in three months. Yeah. Now the, the gene reprogramming gave her a triple lifespan because in that first month, I reversed the cancers significantly to buy us months of life that we wouldn't have had otherwise.

[B]

Right.

[A]

Especially after going through all these other treatments and seeing it just completely fail.

[B]

Right. So you can't say that you failed. You can't, you can't. I mean, you bought her, you, you, you extended her life by at least five months. And, you know, I mean.

[A]

Yeah, we converted three months to basically a year.

[B]

Yeah, yeah, yeah. And not that it's your responsibility anyway, and not that you should bear any, you know, responsibility for anything that that occurred, but you, you, you, you won, you extended her life and, and, and you potentially developed something that could help a lot more people.

[A]

So thank you.

[B]

Yeah.

[A]

You know, it's kind of, it's funny you say this because I, I was watching this cancer convention, A bunch of oncologists with this pancreatic cancer drug. I know how, how they had, how it helped pancreatic cancer patients live some six to 12 months longer. And they were all kind of standing, gave themselves a standard ovation for it. And mine, my gene reprogramming did more than that in a harder case. But I'm like, what is six to 12 months, though, when she's still gone? You know, that's how it feels, though it's not accurate because every day was, every day was meant the world really, every extra day counts. But there's a part of us, and I know there's a lot of parts of other, perhaps widowed parents, perhaps parents with kids that have died or sick that can feel that, like, anger and bitterness at the fact, like, what is six or 12 months, you know, when my person is still gone. But I do also have to remember that had I not given her that time, she would have missed all of the babies birthdays. She caught all of the. Their birthdays that year.

[B]

Nice.

[A]

Because I did that at the beginning.

[B]

Yeah, it's incredible.

[A]

So she was at this point, though, like, at hospice phase, you know, August 23rd, and I'd spent the whole year going back to the beginning of our conversation. I'd spent the whole year trying to figure out how to close that door on the cancer growth. The gene reprogramming, wasn't it? What I had to do was shut down cancer stem cells so we know about stem cells because they obviously create, like, tissue. They rejuvenate parts of our body. But the doorways that create stem cells also create cancer stem cells. So the trick is, how do you shut down cancer stem cells without shutting down healthy stem cells? Okay, which means if we shut down all stem cells, you're gonna. You're gonna really hurt the human, gonna damage the tissue, the gastrointestinal system, because you're stopping cells from being able to regenerate. But if you don't shut down cancer stem cells, you can't really ever cure cancer. Everything is always reactive. Everything is always killing something after it's created. If we truly want to cure cancer, we have to shut down the origin point. And this is the origin point. So I'd been working the whole year at that point on trying to do this very thing. This was my original goal. The gene reprogramming is actually a bigger scientific advance, really, because it goes way beyond cancer. In fact, cancer is the worst application for the gene reprogramming, because cancer is a disease of proliferation, right? It's a disease where cells are created and it takes over the body. Gene reprogramming would really be best in everything else, where the genetic disease is static, where you're not trying to kill tissue, you're trying to transform it. Like you have a severely disabled child, you have a. Someone with Parkinson's or Alzheimer's or something there, where you're reprogramming the gene, you're going to create the necessary conditions to reverse the disease. But in cancer, you still have to kill those cells and tissue. So cancer is actually the least efficient place to have done gene reprogramming. It's actually the hardest place. If it works there, it's going to work much easier in a lot of other places with further development. I've still got a lot of tweaks, but the most efficient way to cure cancer was this cancer stem cell thing. Because if you shut that down, you don't even need to reprogram genes. You're not getting any cancer cells created. And I finally figured it out, but it was. She was at hospice phase. So what happened in August 2023 is I was like, okay, I found this old tapeworm drug, which was approved in 1982 by the FDA for. For gastrointestinal tapeworms. It was called niclosamide, and it hasn't been commercially available for 30 years. They didn't take it off the market because it was unsafe. It was FDA approved. Known safety profile. They took it off because it was commercially just not very successful. Better anti parasitics had come out. Praziquantel for example. But I realized and there were papers from Stanford and Harvard scientists that were talking about nicosamide analogs we'll call them. And those are core drug components of nicolosamide, this old tape one drug. And the Stanford and Harvard scientists, many of which by the way have reached out to me directly and endorsed my paper and everything we're talking about, they were like how come the problem with nicolosamide goes back to what I was mentioning about resveratrol. It wasn't bioavailable. It was, it was like the perfect drug core to stop all this cancer. But they could never get it to work properly. I figured out how to make it work. So what I did is I took the chemistry of the core compound. I worked with Joel's oncologist and I got us. I could only find one pharmacy in the whole country that would do it. But I found a pharmacy based on the oncologist prescription to make. I we re engineered the nicolosamide because of course the niclosamide as it's available obviously wasn't working, but it had something in it that would work. So we re engineered it. Basically half an entirely new drug.

[B]

How did you re engineer it?

[A]

So we basically had to improve its delivery system. So we, we basically in the pharmacy process we had to create things to make that drug travel through the body better. So we had to add in different ways of, of making it bioavailable. I. We did. And unbelievably in that weekly biopsy that came back after weeks of it going up, those cancer stem cell paths were completely eliminated, gone, dropped off from the blood completely and the tumors halved in a week. Wow. In like the most ultra aggressive, lethal treatment resistant possible cancer case.

[B]

This is undisputed results.

[A]

Yes, it's so Tempest Labs for those that want to go look at my paper, you'll see it's from Tempest Labs which is the number one oncology lab in America. If you, not you. But if someone has cancer today and you go to your oncologist, your liquid biopsies are going to come from Tempest Labs just like mine. It is the gold standard used by all oncologists across America. Yeah. So it's, it's like you could not ask for better independent verification because it's the one your oncologist uses. I was a husband, I had to use the things that everyone else has to use. My data had to come from the same system that everyone else's came from. I didn't have a private lab or, and that's the wonderful part about this story, Is that all of this is so independent. Like, not only was there a step between me and the doctor, There was a step between me and the doctor and the lab. And all of these are independent steps. The doctor verified my thinking and my therapy, and then the lab verified his sending for the results based on my therapy. So we have multiple points of independence on top of that. Like these liquid biopsies are signed by multiple doctors, not just the oncologist, but there's a medical Doctor and a PhD, etc. All doing it in the facility. So we're talking multiple medical doctors involved in just one step of data verification. It really is as objective as could possibly be. Far more than most case studies that are published, because those are usually coming from doctors who have written them directly and usually coming from labs that like their own hospital. Whereas me, I wrote it. A doctor was in between, and then the lab was completely separate from the doctor and from me. So we have way more steps of independence and verification here. We also have during this cancer stem cell elimination part, we have a hospital the surgery Ki67 went down. So the Ki67 is how fast cancer cells replicate. That was down. We have circulating tumor cells, the tells, the cells in the blood that are being shed that came down hospital CTCs and the tumors and cancer stem cells were all three separate labs all at the same time. So all showing everything going down. So it's as robust as could possibly be. And the most amazing part about this though, was that I finally got to the core engine of what made cancer work in every cancer, not just yours. See those tumors, like those receptors and stuff we were talking about, that's specific to this cancer. But the cancer stem cell pathways is every cancer. Yeah. Doesn't matter if it's glioblastoma, colon, pancreatic, breast, all cancer uses these pathways to generate. So if we are able to cut the regenerative engine at the root, this truly is the closest to a cancer cure proven in a human that we've ever had, because it's the only thing that can universally apply to all cancers that isn't just dependent on a specific type. Now, it would. I want to be clear that it wouldn't be in of itself a full cancer cure. It is cutting the re engineering. It is cutting the regenerative engine of cancer. So what that means is we're not eliminating all cancer for everyone with this treatment, what we are doing, is putting the cancer in stasis. We're eliminating the cancer's ability to metastasize, to grow, to spread, and to keep coming back. So it's much more equivalent to. Think of it like, like a diabetes treatment that keeps insulin in check. You can live a pretty functional, normal life. And I know there's better ways to do this, but what I'm just as an example, think of the cancer stem cell elimination. Not like an absolute cure, which it isn't, But a way to keep cancer paused. Yeah. So then you have time. You could chip away at the tumor with all sorts of things for months, years, because we've removed the ability for it to spread and keep coming back. So really, I would see the cancer stem cell elimination as the foundation. If we can reproduce it and take these molecules, make sure they're still safe, reproduce it across cancer patients, then it would be the foundation, really, of all cancer treatment, Whether you have pancreatic or not. Because this removes that doorway that allows these cancers to be created. And then each cancer type will have specific things that help them on top of this. So I would really view this as like an adjunct to kind of be the baseline underneath all those specialized treatments for those specialized cancer types. Yeah. So they're still going to need their other things, but this is the key to giving them many years of life While those other things work. In other words, I think this drug, if we can, If I can do it the same way or improve it from what I did before, it would make all the other treatments actually finally work. Yeah. Especially in these treatment resistant cases. Because of like 50 million cancer patients a year, 90 of the deaths are treatment resistance. And that's this cancer stem cell problem. The cells keep coming back. If we eliminate that, we've got, We've got time. Because one thing that Jill's case showed me is time is the biggest enemy. You know, I finally figured it out. If I'd done this part at the beginning, she'd be alive because I would have been able to eliminate the. The super fast growth and eliminate the cancer's ability to keep growing back like it did on the breast. And then we would have had time to chip away at those tumors. If I'd done this six months earlier, she'd likely be alive.

[B]

So this, I mean, this process and, and the technique would. Would work for anybody, I guess, right?

[A]

Yeah. Yes, it would.

[B]

Because my, My aunt died of pancreatic cancer a number of years ago. And you mentioned Alzheimer's before My dad has that right now, so. He does. Yeah, yeah. He's in late stages on Alzheimer's, so. Yeah, yeah. It's tough for, for everybody.

[A]

Both diseases are miserable, very different reasons. Yeah, yeah. And it, it, there's, there's little more miserable, I think, than watching someone you love much degrade like that.

[B]

Right.

[A]

I, I right. You know, the, the key to the Alzheimer's and, and the, the, all of the, the, the genetic diseases at large is, is really my son, which we'll come to, I guess more than Jill's case. My son is really the key to, to those problems. Jill though did prove that it change gene expression without hacking up the genome and editing it. You know, so, and that's, that's the most profound part of the gene reprogramming is that actually they didn't know it was possible to change gene expression like this, especially genes that are completely undetectable, to switch them back on with molecules. They thought that would be like, you know, woo woo kind of stuff. But here we are. It is possible. And that's the most important part about what she gave us. But as far as cancer specifically, this cancer stem cell elimination drug that I need to develop is the key to cancer specifically. Okay, yeah. This is the gene reprogramming is the key to everything else but the, the cancer stem cell elimination drug. If I'd done it early, if I'd reversed them and done the cancer stem cell at the beginning, she'd be alive.

[B]

Have you published any papers on this?

[A]

Yeah, yeah, this paper's published, this one's published everything we discussed. Yep, it's. So the, the thing is, is peer reviewed. Yes, well, by the doctors openly, not in a journal. This is the one. So this is on Research Gate. And then the reason that we didn't. Now actually I haven't resubmitted this to a journal recently. So Research Gate is like a pla, an academic platform where we have papers. And this is in Google Scholar.

[B]

Do you want your email address on the episode?

[A]

Yeah, that's fine. Yeah. So this was peer reviewed openly. So for example, I had Dr. Erin Greer from Mayo Clinic peer review this after I published it. It just wasn't peer reviewed in a journal. And the reason it's not in a journal is because they wouldn't accept it because I, I did a human case without a review board approving it.

[B]

Okay, gotcha, gotcha.

[A]

As if I had time for a review board while my wife is dying.

[B]

Right.

[A]

You know, but, but that, but that's the law. Like most of these I, not the law, the regulations. So when I submitted this to multiple journals, they kept bouncing it back by saying any human study needs to be approved by a review board. And I was like, I mean, where we, where do I even begin with that? As if I had time, as if it, as if it even is necessary ethically.

[B]

Right.

[A]

When it happened to us.

[B]

Right.

[A]

But that's part of the thing. Then there were other journals which wouldn't even let me submit it because I didn't come from. I didn't have a. Edu. Email.

[B]

Wow.

[A]

Yeah. So what I ended up doing is finding doctors independently to peer review it after I wrote it.

[B]

Okay.

[A]

And then, so I, I, There were a couple of Doctors. There were four in total, actually. But Dr. Greer is the only one that has allowed me to talk about her publicly. That's why I focus on her. She was, she's a, she's a precision oncologist, but she was a doctor at Mayo.

[B]

Okay.

[A]

So. Yeah, and, but honestly, it's been open, peer reviewed. I mean, gosh, thousands of scientists have read the paper. Some hate me for it, some love me for it. You know, what is that?

[B]

What is the hate that you get? What's the pushback or the skepticism or whatever? What, what are, what are they. Yeah, what are they pushing back on?

[A]

Yeah, the, the. So they. Well, it depends on which layer of analysis we're looking at. You know, from, from the perspective of. If I'm going to give them credit, let me. They're pushing back on the fact that these results were such a narrow window that we, we didn't, we didn't get to view them consistently. So that their primary skepticism is. It's too much of a fluctuating result. Like one snapshot here, one snapshot there, that doesn't really tell us much is their kind of primary skepticism. There are this, There are other things. I like the difference between liquid and tissue, but I've already addressed that. The differential there is minimal. But the snapshot part, that only works if you're not taking into account that we had weekly results prior to my interventions where the tumors were going up. So then I'm now supposed to believe that my one intervention, where everything completely disappeared is what. Not because of my intervention.

[B]

Right.

[A]

Then why was it going up through all the other treatments every week? So it's, it's kind of silly to be honest. Especially because if these scientists are truly serious, they would know that I'm basing this targeting on known molecular oncology based on known drug compounds that target these areas Based on papers from Stanford and Harvard.

[B]

Right.

[A]

You know?

[B]

Right.

[A]

And they're just not happy that it was a father outside of the system who did what their Nobel prize winners haven't done. That's the truth. But as I tell people all the time, if you're angry that I surpassed your Nobel winner, then you're thinking through the long wrong lens. I lost. I didn't win. I lost. Give me back Jill and you take the results. I'd happily do that. You take the gene reprogramming and give me back my wife.

[B]

Right.

[A]

I didn't win. I lost.

[B]

Yeah.

[A]

The problem is they're looking through the lens of thinking that I. That because I did something that is so advanced that I, They. They're trying to, like, take it away from me is like, there's nothing to take. I already lost.

[B]

So what is it that needs to occur in order to push this to the next level? To be able to make progress, to be able to show that this can happen in more than this case and that progress can be made and that this is an effective treatment?

[A]

Yeah. So we. I'd been. I had. We need investors to fund a patient program for the cancer treatment, specifically the gene reprogramming as well. But I need to do more, like, real deep work on the gene reprogramming, like, more like the cancer one. We could start with patients like today. The gene reprogramming, I need to run through some pre clinical first because I need to make sure that the updates I'm making are gonna work. Needless to say, I had conversations with many investors. I had one guy in the UAE who was worth 64 billion, who wanted to move me out there, but they would own the intellectual property. And I was like, I cannot hand over the keys of the genome and a cure for cancer to. To someone that we could not possibly. I believe, from a spiritual perspective. I was landed with this because I understand the cost of it. I understand the. The emotional cost. I understand the price that has to be paid for doing something like this, and I understand how to steward it because I have lived the worst of it that other people have to live. I don't. I don't want to keep the intellectual property to myself because I want to be a trillionaire. We have to steward this properly. We can't push out a cancer drug that could save 10 million lives a year and sell it for a million dollars or whatever other issue, or even worse, put it in a box away somewhere, you know. So the problem is, I had investors come in some Were great, some were not, but nothing mission aligned. So I'm still hoping that we'll find our mission aligned investor for the patient program, but we haven't found one.

[B]

So what does that ideal situation look like from an investor standpoint for you?

[A]

So the investor would come in, they'd own a piece of the therapy. Right. So they'd have like that piece of equity in the company. They'd have a piece of the therapy. We would do a small patient program. I would a dozen, two dozen people, treatment resistant cancers. We could do it as part of conventional care. So the goal of this is to make the conventional care work like I mentioned earlier. So from a legal and ethical standpoint, it's completely flawless because we're not pulling them away from anything they're doing. We're just going to go in and make their treatments fully work as an adjunct. So it's perfect. And honestly, we'll save millions of lives per year if we can pull it off. So it's a small patient program. I have a clinic, have a doctor's, just didn't have the funds yet. Yeah. So that now in the gene reprogramming, much more important. But I realized that the original version I created in Jill's case won't work because of that whole energy problem I mentioned. So my son has been the key to figuring out how to surpass that. So Jill's legacy is going to be we kill cancer. My son's legacy is everything else. Everything else, you know, everything genetic really. So the problem with the gene reprogramming is we are nowhere near as ready as we are with cancer. We could, we could run through the cancer as soon as possible, you know, so that's the situation. So that's why we haven't been able to move forward faster. And I'm still, still waiting. Yeah.

[B]

And what type of funding? I mean, how much funding do you need in order to, you know, be able to make the type of progress that you want to make?

[A]

Honestly, we could do a dozen patients for like 5 million, which, given we've already got a human proof of concept, is super cheap and conservative because most human proof of concept like this is usually like series C or D. And I did all of that myself. So, yeah, it wouldn't be big bucks. At least the. That's why I wanted to focus on like a dozen patients. Because then once we can reproduce it through a dozen, then it's like, okay, now we can do big. We know it's going to work across a hundred, so we can do Big investment. But I was just kind of going for a smaller initial investment to. To make sure that it works. Yeah.

[B]

Yeah. Fascinating. Okay, so. Yeah. How old are your kids today?

[A]

Yes, mine and Jaws three. So it's four, five and six. And the six year old, six and a half Aaron will be now, is now the, the center of our. The center of our story.

[B]

Okay. Yeah. Do you want to maybe take a break and come back and pick up the story there and finish off on the, on the second half discussion kind of next? Yeah, good. Okay, we'll take a quick break. I think we just pick it right back up. We were going to kind of start off going into your next mission which involves your son.

[A]

Right, right.

[B]

Yeah. So how do you want to kick? You go ahead, dive right into it.

[A]

Yeah. So Jill and I had three children. And the youngest, sky, has severe autism. Like non verbal, like very low functioning behaviors. Super like sensory processing issues like sleep disruption, eating issues, like really severe level of disability. Aaron, my son, the oldest of the three, he has all those and so much more. So I noticed about two years ago. I started a year after Jill died because it took me some months to even look at this stuff. I was just like, just emotionally devastated. You know, I actually got like physical heart problems. Like I. I got a literal broken heart. So I got. I had to wear this like beeper. They scanned my heart for two days. I got diagnosed with ventricular and atrial depolarization. So heart contraction issues which happened the day after Jill died. No heart problems ever. No genetic heart problems in the family. It literally happened the day after she died. So I got this heart issue and I was in a. I was in really bad shape. I couldn't eat. I didn't eat for like two weeks, three weeks. I dropped down to like 115 pounds.

[B]

Geez. How tall are you?

[A]

5 10.

[B]

Wow.

[A]

Yeah. And the thing is, is the I will happened in just the first few weeks after she died. So it like it hit me really hard, really fast. And then I realized because I had these small children that I had to find a way to live. I had to find a way to survive. I somehow kind of pulled through it all through kind of what we talked about the beginning. I realized that I had to feel the emotion. I had to feel the pain. The only way out was through.

[B]

Right, Right.

[A]

Reminds me of what Jung said, you know, the in filth it will be found is something that Carl Jung said. What you need most is where you least want to look. The irony and the seeming paradox is the healing had to come through allowing myself to be broken. Right. So after I just let the sadness come. This was about six weeks after she died. And it was like Christmas Eve 2023. And it was like the worst moment of my life because it. The reality hit and I'm like, here with babies on Christmas and it's just me. And it just like floods of tears came through and they didn't stop for many months. But then in that journey, I started to be able to eat again, you know, and I started to be able to. My heart problem started to get better as the emotion could work itself through, you know. And then I realized that the whole point was that I had to feel the thing that I really didn't want to feel, the reality of what happened.

[B]

Right, right.

[A]

What is interesting is I didn't know we were talking about it before, about the cancer stem cell elimination. I didn't even know we'd done that until two years later. I had the medical records, but because Joe was at hospice phase, I wasn't actually looking at the medical records anymore. I was. It was at this weird transition point where I had this last attempt at therapy. And then she was in hospice and just declining. And I wasn't actually checking the records. We had them. The doctor would send them to me every week. And then as I was writing the paper two years later, I had to go back through the records to write the paper and make sure his course it was accurate. We. And that's when I saw that I'd done what I had been intending to do that whole time. It was still too late to save her. Wouldn't have mattered had I known at that point because her body had been completely destroyed. But it just kind of goes to show that even like curing cancer functionally, meaning putting it in stasis, didn't, wouldn't. It wasn't even on my mind anymore. You know, at that point I was just a grieving husband and father. So about a year of deep grief that frankly would have lasted a lifetime had I not let the tears come through. But because I let them come through so consistently, I managed to move a lot in a year. And then I started to work on the severe autism for my children and started looking at how I can convert some of this gene reprogramming to. To reverse an act, because only about 20 or 30% of autism is actually genetic. Now the hospital, Sanford Hospital, big hospital in, in the Midwest where I live, they. They said that only 20 of their children who have diagnosed autism come back with Autism genetics.

[B]

Okay, I didn't know that.

[A]

Yeah. And the thing is, on the wider level, I think it might be more like 30%, but most of it is not genetic as we, as most people think of genetic. Most people think of genetic as DNA. So if you think of the DNA helix at the core of a gene and then over the core of the gene you have rna, you have protein, you have histones, etc, etc, you have all of these layers on top of the DNA and all of those layers combined are what make a gene. So the DNA is just the bars, the nucleotides at the center, but the gene is actually all of the material on top. So if we think about that, 20% of autistic children, like my children, they have it at the DNA level, whereas the other autistic children, they will have genetic components, but they won't be at the DNA level. So they'll have pieces on top of that DNA, such as that gene silencing, those genes being tight. But as I kind of demonstrated there in Jill's case, we can switch those back on without changing DNA. So for the vast majority of autism, we can reverse that like completely with developing this further at the DNA level. It's tricky. Now what I've done is look at how I can convert this for my children. But then I did the genome sequence for my son to find out. Okay, so if we, if I'm going to target and try to reprogram gene expression, I need to know exactly where the genes are coming from. Because autism is honestly one of the most complex disorders and diseases. It's very heterogeneous, which means it can come from dozens of genes and it involves an entire network within biology. It's metabolism, it's biochemical, it's genetic, it's, it's everything. It is an extremely complex system. So I did the whole genome sequence on Aaron and then we went to the hospital for his genetic testing and stuff. But what I realized is that Aaron, Aaron started, his vision started to go. He was like losing his eyesight slowly. He was having problems with his ears. He's non verbal either, so he can't communicate to me what is happening. But he's like constantly trying to do this. And we had his vision tested, his vision is going, he's obviously having hearing issues. His gastrointestinal system started to slow down, like it just wasn't working well anymore. And then what I realized is that Aaron had a number of very severe genetic problems, not just autism. But honestly there's, I've never heard of or seen anything like it. Aaron has hundreds of genetic mutations. Even if we take Jill's like ultra lethal cancer, she had half a dozen, maybe let's say five inherited mutations that kind of underpinned her ultra lethal cancer. Aaron has four times what Jill had from birth. What it's called in. If we kind of take all of Aaron's different genetics, we have a couple of different conditions. There's really nothing like it because I explained, I think in one of the news articles like it was Benzinger I think or something. But I explained it in that, that to the journalist there that Aaron has a collapsing genome. You can't really think of Aaron as a disease. It's just that there's so many structural weak places that the, the architecture of the genome itself just can't hold because some genes are more critical for function than others. And he has broken genes in so many functioning areas that it's not really, he's not really going to die of one disease, he's going to die of a dozen. As they're all starting to cave in on themselves. The pressure cannot maintain it. Now from a. To make it kind of simpler for people, there are very, very rare like one in a million terminal conditions in children that are pre cancer. There's one called cmrd, Child Mismatch Repair Deficiency. And I talked about mismatch repair genes. In Jill's case, what it means is that children who inherit these mismatch repair genes, genes that repair DNA, they're missing them or they're broken. So they are guaranteed a pediatric cancer. So it is like a one in a million terminal condition, even pre cancer because they don't have the material to protect against the cancer. So the cancer is inevitable. 100 pretty much, yeah. Yeah. And then on top of that, he has actually two or three of those various pre cancer terminal conditions where honestly he shouldn't have made it past infancy. The fact that he's made it far enough for me to do anything is a miracle. He's already bypassed one in a billion odds to get here, which is what actually gives me hope because I know if he's made it this far, Aaron's odds to survive this far as I would understand them, and I feel like I'm qualified to understand this, he has beaten odds Jill would have beaten to live already by like a large number because even though she had a more aggressive active disease, his architecture is far more complex and broken at far more. Like if you think about it this way, she had working architecture in other parts of her body. Outside of this tumor tissue taking over her system. But he doesn't. His architecture is broken in critical parts everywhere from baseline. So even if I were to like cure the cancer, there are other parts of his healthy tissue that can't actually defend him against that anyway, where she had a chance at that. So in addition to that, we have, he has something many, many, many broken parts. But we have like neuron death, slow neuron death because of a lack of energy like glucose, hyper metabolism, insulin issues. But the primary one from the cancer is the, is als. So he has a, what's called a gain of function, a frame shift in the ALS gene. So typically what the way that this would work is if both parents copies are completely toxic, then the child would die in infancy of ALS because he has one toxic and one somewhat working. Then his would be early adolescents, late childhood, and not infancy. In other words, that second one is bought maybe 10 years. Whereas if both of both copies were gone, he'd have died of the ALS in infancy. So essentially we have multiple cancer syndromes, we have many forms of neurodegeneration, but the most toxic and like genetically clinical one would be the als. But it's really not really als. It's just a compounding failure of too many weak points. I just wanted to kind of put it down to two things that people could pinpoint so it's easier for people to understand.

[B]

And ALS is Lou Gehrig's disease.

[A]

That's right, yeah. Yeah. So it's like total motor neuron failure and the, and the inability for the neurofilament to actually create the right material to even axonal growth, synaptic growth.

[B]

That's Michael J.

[A]

Fox Parkinson's.

[B]

Parkinson's. Oh, okay.

[A]

Yeah.

[B]

I don't know why I thought so.

[A]

The, the ALS is kind of where the whole body just starts to break down and it is neurodegeneration, but it kind of goes through the spine and everything else.

[B]

Okay.

[A]

But in Aaron's case, it's still not really that. It's still really a collapsing system. That, that and the cancer are just the two primary drivers, but it's really a whole network of failures that will be pulled down with it. So if you think about Jill or any severe like ultra deadly disease as like a burning building and you have to go in, you gotta blow out all the fire and pull the people out. Aaron isn't like a burning building. He's an extremely unique case. He's like broken windows, infestation in the walls, sinking into the ground, and a Storm is coming. Completely different kind of problem. Which is why that Aaron is the key to everyone. Because Aaron has these. These compounding failures are also linked in Parkinson's and Alzheimer's. Like, he has the. He has like, the apos, the pink ones, and all of these, like, different genetic disease components, which would be benign in his case if he didn't have these other things pulling it down.

[B]

Does he have two copies of the APO? E4.

[A]

No, he's just got the one. Right. Which, which kind of goes back to the whole point in Aaron's case, which is unique. He's got a single broken copy across most of these, but because he's got a few really critical broken ones, the others act like compounding failure. Like, they escalate and accelerate the failure. Whereas if he just had apo. Just had the Alzheimer's, he wouldn't. That wouldn't affect him until he was 70. But because he's got all of these severe genetic disorders pulling it down fast, it becomes another point of accelerated failure.

[B]

Right, Right.

[A]

So most of those genes in Aaron's case are not deadly. They accelerate what is deadly and make it much faster and harder to stop. So, and I could list dozens of them that are in this case, like insulin failure ones in particularly specifically neurolog, collagen failure, visual cortex to eye to retina, Wolfram syndrome. Like, again. So we have, if any of these were individual, Aaron wouldn't feel them until he was much later in life. But they're in a system where we have either toxic or failed genes with accelerated pediatric mortality. So then all of these begin to compound and accelerate that failure. So then it's not just a matter of, like, ALS or ultra lethal metastatic cancer, but actually the insulin levels in the neurons are not getting enough energy as well. And the collagen in between the eyes and the brain is also not being built as well. So then you have all of these things compounding, and then that's why it just starts to sink. So in Aaron's case, we cannot save him by just restoring an ALS gene or by just restoring a cancer gene. We have to essentially normalize large amounts of the entire genome. We basically need to restore a dozen to two dozen different genes on different chromosomes in different organ places. And honestly, doing a dozen isn't actually much different than doing two or three dozen because of the interconnected network I have to use. Think of it like the house is sinking, the windows are broken, your termites in the walls, and a storm is coming. And if I had to get A crane to go under the house and lift it up and build protections around it. Well, it wouldn't. With that much infrastructure, it wouldn't make a difference if I had to do the next house next to it. The hardest part is actually getting in and doing it. Now, in Aaron's case, we don't really know how long we have. The truth be told is he really should have had an ultra metastatic cancer already by normal, conventional understanding. So, you know, tick tock goes the clock. The neurodegeneration is more predictable and slower. I would say we probably have like five years of a kind of predictable collapse. But in the. On the cancer side, I mean, it could literally be triggered any day. It's so volatile. So I've got to work pretty fast, you know, and I've been trying to. But he is a very complex case. The most complex case by far. You know, what is his quality of life like.

[B]

Like today? I mean, what is he. What is he doing? What's he, you know, like, is he going to school? Is he. How old is he again?

[A]

Six and a half.

[B]

Six and a half.

[A]

Yeah.

[B]

He.

[A]

His quality of life is. He's still pretty good. He's still. He's in way better shape than he should be. Okay. Yeah. Like, I'm not saying that he should be a hospice right now, but given the genotype and given the activity of these. These breaks, he is way better off than I would have thought.

[B]

Good.

[A]

So his quality of life right now is. Is pretty good. He. He has very severe neurodevelopmental disorder. He also is starting to lose, obviously, some function. Like, we're seeing cerebellar issues as well, like tripping up occasionally, but overall, he's still pretty functional. No good.

[B]

And the doctors he. I mean, you're working with traditional doctors that. That are.

[A]

No, no, no. I did see traditional doctors, but that, aside from surveillance, like, to make sure that no metastasis is opening up. This is not a problem they could even begin to solve.

[B]

Okay.

[A]

Yeah. Not. I mean, they don't have. They don't even have a 1% chance. They have a 0% chance.

[B]

Right?

[A]

Yeah. An absolute zero.

[B]

Okay.

[A]

But I do have. I mean, I. I've got hundreds of doctors who support me and who are. Who are in my circle, who I consult when I need to about stuff. But the truth is, is that the only way Aaron lives is if I make it happen.

[B]

Right?

[A]

Yeah.

[B]

Yeah. Yeah. My son's six and a half as well. That's right. So what. What does he know? Probably Nothing of what's going on. Right? I mean. Yeah.

[A]

Nope.

[B]

Right.

[A]

No, nothing. It's kind of a. It's an interesting thing. And, and, and honestly, that's kind of more the. That's more the severe disability, the severe autism, where he's kind of in his own world. He is not really. He's not really aware of what's happening. You know, he's not really aware of. Of the environment. But I do think there's something. I'm gonna sound crazy again. They'll write a whole new Reddit thread about me after this podcast because they'll be like, mark. Mark Malone is insane. But I do think there's something deeply spiritual in children like this, especially him. I remember when Joe was dying, Aaron, I had her at home. I only took her into hospice the final week of her life, and in that final week, it was just me and her there. That's what she wanted. But in. I had her at home up until that final week, and I would take care of her. And the day before she went into the hospice facility, Aaron jumped on the. The bed. He was only three. The other two were super little. And he, like, grabbed her head and, like, screamed at her face like this. He'd never done that before. The thing is, is that I took her into the hospice facility the next day, and he never saw her again and never would, but it's like he knew I didn't even know I was taking her into the hospice facility the next day. And it gets even weirder because the day she died, November 2, exactly a week later, he was in school, and she. The teacher messaged me and said that he was, like, pulling teacher's hair and scratching and screaming. Never done that before and never done it again. Only did it the day she died. But he didn't even know she was dying in the hospice. But he did.

[B]

Wow.

[A]

He could feel it.

[B]

Yeah.

[A]

And he was very, very, very, like, tuned in energetically. Whether we look at it from a perspective of psychic or whether we look at it from a perspective of the fact that as a. As a. As an autistic brain, he might be bypassed on the prefrontal cortex, or even the whole neocortex area might not be working so well, but the truth is, is that he's actually banking a lot more subconscious energy than we think. Or rather, he might actually just be absorbing a lot more, like, peripheral energy that he can't contextualize and understand, you know, but whichever way it is, he definitely is tuned in energetically, and I think he's he's, again, might sound crazy, but I think he knows, like, what he is here to do, you know, And I think we're gonna succeed.

[B]

Yeah. That's fantastic. Well, yeah. So what are the next steps then? Like, what are you. What's your. What's your plan? What do you. What do you have kind of, you know, coming up in terms of how. I'm sure you've got a. You know, things that you need to accomplish in a certain amount of time, and you've gotta. You've got a planned out, you know, documented. What. What does it look like?

[A]

Yeah, yeah. So we have. So I have, like, three primary tracks that I have to run in parallel that are completely separate. The. The gene reprogramming that we started in Jill's case, that I am developing further in Aaron's case. If we succeed, we're gonna be able to essentially restore, without editing, DNA, even the worst of genetic disease mutations. Because the whole idea of a mutation is that because the DNA sequence is so off, like in Aaron's case, we're not just dealing with, like, silenced genes like in Jills, where we need to remove that material and get them back online. The actual DNA sequence at the core of it isn't working. But I think that so much of the core of that DNA sequence that isn't working is because of the very material on top of it. In other words, the gene as a whole, not just the DNA. So I still think that what Aaron is going to allow us to do is even when there are real structural DNA problems, the gene will still be able to express itself to some normal degree. And if we do that, then we take this whole thing to a whole other level, because then we're not just switching genes back on, which already is like a billion people's disease, but we're actually able to take DNA communication issues to that gene and make them start to express themselves normally. Because in Aaron's case, I have to do that. So the goal with the gene reprogramming as track one is for us to continue to try to develop that. Continue to try to build what I learned after I did the first version with Jill, which is like, how to make. How do you change the metabolism of disease cells without breaking it in other cells? All of that stuff. And in Aaron's case, we have to basically light up the genome like a Christmas tree. We have to switch on lots of parts and places in different regions of the brain, in different organ tissue. And I think we can, because we already did switch genes back on in different tissue types across chromosomes. But now we have to do it at a bigger scale. So we're going to be running that. And then aside from that, we have this cancer stem cell elimination which we have to do. And I want to get that into a patient program as soon as possible.

[B]

Right.

[A]

And then on the third track, I'm trying to do something like more decentralized. We have a little crew working together to try to do something that we can do like direct to consumer, that doesn't require like a deep drug or deep FDA kind of process because the cancer drug is going to be safe, is going to work tremendously well. But even then, it's still three years best case to get it like out to the world because that's like the fastest they could move it in FDA pipeline. So let's say over the next three years we can continue to do those patient programs, get the data, and then three years from now, the world finally has a core cancer drug that can work for everyone. The gene reprogramming. This is the apex of all bioscience. This is the apex of every everything molecular science at all. Because this is the vast majority of disorder and disease that might take longer, But I do think that again, Aaron is going to give us phases. So the way that I view it is that next year we'll have like a cluster of disorders we can solve and then a year after that we'll have another cluster. And as I continue to crank away at this for Aaron, he'll give us a whole new cluster of diseases and by the end of it, five years from now, we'll have Alzheimer's, als, Parkinson's, severe autism, rare chromosome disorders all mapped out and ready because we're going to do that through him. And then the third one is this direct consumer thing where that'd be great

[B]

because I, I also have that APOE4 gene, that Alzheimer's.

[A]

Yeah.

[B]

Gene. So yeah, get the work on that one.

[A]

We'll solve that one. That's, that one's going to be one of the easier ones actually. The, you know, the Parkinson's and the Alzheimer's. I, we, we've mapped out a lot of this already and that the hardest disease category is actually something like als where it's. The problem is the gene is producing toxic protein. So the gene is toxic. Whereas in a lot of the other disorders, like in Parkinson's pink one is often like shut off or under producing protein. What's called a hypomorphic mutation where the gene isn't producing enough sequence. Like it's not like it's not protecting like the cancer gene. It's not sending the protection sequence

[B]

through

[A]

Jill and Aaron, mostly through Aaron. I already have the path to getting those genes back online, if any. If, if we can get someone who doesn't want to take me as a slave to another country to fund it, we'll be able to get those genes back online. The hardest category, the two hardest categories is this like toxic one, because we're not trying to improve function. There's. The function itself is inherently broken and bad and that's like als. The other hardest one is the children like Aaron and Sky and other children that are born with rare, rare genetic chromosome disorders because it's like deeply baked into the cake. You know, it's like they've come out that way. Some of them, like they have genes completely knocked out, some cases deleted, which is the hardest one of all. So those are like the two hardest categories that are going to be the long, the long run. But I think along this journey of the next couple of years, if we have the infrastructure to do it, we're going to be able to switch on some of these like the Parkinson's, the Alzheimer's and even some forms of autism for sure. But the cancer one is I, I would prefer to be the public priority, even though my priority is save my son. Because it's like, it's something we genuinely could do like as soon as possible and it doesn't require waiting for me to, to invent new things. Like we can just do that. And it is one of the worst diseases known to human history and it would be nice to finally eradicate it and get a handle on it. The direct consumer thing I'm trying to build because I don't want everyone to have to wait years for help and intervention. So I try. So through my youngest daughter, sky, because she's 4, I was like, and she's not terminal. I, I would, I, I was like, I can't bombard the girl with you know, pharmacological agents and like her life isn't at stake and she's super small. So I was forced to go completely outside of like drug territory and think completely outside the box. And how can I get a bunch of, how can I design like nutraceutical agents that are like super low risk and appropriate for a four year old, but that would reverse something as deep as like a, inherit like a genetic autism. And that's what I spent most of. In parallel to Aaron's stuff, I spent most of the year working on that. And I've, as of just the last couple of weeks finished designing it. So we're going to have a, like, essentially like a nutraceutical formulation of a number of molecules and compounds that would be legally and ethically able to go straight to the consumer. No FDA approvals or anything. I'm using things that have already known safety profiles and things. We've improved the delivery system on all of them to make sure they actually reach their target destinations like I did with the drug. And then we can get that straight to the world. And that could be done in months. So that, so those are the three tracks and that one was important because I have so many suffering people that want help and I'm like, I mean I. A drug path is a drug path. I can't make it any faster. But this is something we can do fast and get straight to the world. And this would help with a lot of conditions because this isn't like a deep gene reprogramming or like, you know, curing cancer. But what it is going to do, if it works as well as I hope and designed it, is going to shift gene expression. But it's not going to shift it so hard where we would require deep pharmacological agents. It's not going to shift it so hard where we would need to monitor the gene expression. It's only going to work within what biology would allow naturally. So for example, we know like with the, with the fasting and we had to use some of that, in Joel's case with that glucose glutamine starvation of the cancer cell that helped induce epigenetic expression difference as part of my triune system. It was a part of that metabolic pillar of the three pillars. And of course that's available to anyone to do anytime, anywhere, right? It's not a drug. The point is, is that there are ways that we can shift gene expression naturally, safely, within reasonable limits. We can't gene reprogram, we can't cure cancer, but we can make the cell more permissive to expressing itself in a healthier way. So the nutraceutical delivery and optimized delivery that I'm trying to make, I made with the safety and efficacy of a struggling four year old in mind. So it had to work and also be safe. Because if it ain't gonna work, it's a waste of my time, it's not going to help my daughter. But if it's also, if it's not safe, I can't give it to her. So I think it's gonna have tremendous impact. One of the most amazing things about it is it's going to essentially reverse the core inflammatory signals that shoot in most disease. See, in the brain of a neurodevelopmental child, as severely autistic child, there is a lot of metabolic and inflammatory problems. There is, there are things like calcium ion overload between like CA1 neurons not getting enough, CA2 getting too much in the hippocampus for example. And then these are causing like inflammatory cytokines like interleukin 1 beta, interleukin 6 whatever tumor necrosis factor alpha. And these cytokines are causing like basically brain inflammation. But interestingly enough, if you get like a viral infection and your body starts to over fight it and we start to die because our body is fighting so hard, it's the same inflammatory cytokines, things like interleukin 1 beta and interleukin 6. So by sort of reversing this brain inflammation, we can also reverse a lot of inflammation for all sorts of conditions like arthritis, lupus, long Covid and we can do it safely and direct to the people. I'm by no means saying it's going to solve all of these conditions, but I expect that it will help tremendously. Yeah. So that's the goal with that and, and that's primarily kind of regulating the cellular environment to fight inflammation related disorder, which is a lot. It's a lot. Yeah. And I think it's going to do a really good job of that. So that's going to be the thing that the world gets fastest. And you can thank my youngest daughter for that because she forced me into this other box of what can I do fast that's safe and effective. So you see, each person of the family has given the world something new. Jill gave the world the path to curing cancer. Aaron is going to give the world the path to broad spectrum genetic disease therapy. And Sky's given the world safe direct to consumer therapy. You know, Nice. They've all played their part, I guess.

[B]

Yeah.

[A]

You know.

[B]

Yeah. Inflammation is such a, it impacts so many people and so many people don't realize that, that they're being impacted by inflammation. It's I think the last three times. Well, I got a, I got a blood test done and so it measured all of the, it was like seven vials of blood. I was doing a 10 day fast and I didn't realize that I had an appointment on the 10th day to get blood drawn. So in hindsight I probably would not have drawn seven vials of blood on the 10th day of a 10 day fast. I was not in a good mood after that, but trying to take a walk and was, you know, like falling on the street, but not falling, but sitting down. But that told me all these things that I had histamine responses to all these foods. And so, you know, when you go to an allergist and you get tested for things and it's not food, it's always just external allergens, dogs or dust mites or dust or whatever it is. But this was a fantastic one because you were able to test for foods and that's really what, for the most part, keeps people in this inflammatory state. It seems like that's a major part of what's happening in America with people being inflamed. It's because we don't realize that we have these histamine responses to various foods. Mine's like pineapple and strawberry and brussels sprouts and tomatoes and eggs and milk, dairy, you know, just all these things that I just, when I stop eating them, my inflammation just goes away immediately. But I think the last three times that I've felt like I've had no inflammation is travel to Europe for like two weeks. Because the food there is just sourced differently, it's grown differently, it's cleaner. And then this fast that I did, I mean, inflammation within 24 hours of not eating to, you know, 48 hours, it really goes away. That's when all of your inflammation is gone. But you're right, it's such an important part of the health of everyday people, specifically Americans, because of diet. And it's just something that people, you know, we're hooked on this food system and it's like the way this stuff is made is just so, you know, toxic for people. And it's the cause of so many different types of diseases. I just felt compelled to mention that because for anyone who doesn't kind of realize that a lot of your inflammation is coming from things that you might not even realize you're, quote, unquote allergic to or you have this histamine response to. And I just encourage as many people as possible to go get tested for that.

[A]

The histamine one's an interesting one. Yeah, because histamine is also a neurotransmitter. People don't know that, but it's, it's a neurotransmitter of like, mood, just like serotonin or dopamine. Histamine responses, like histamine receptors, like 1, 2, 3, are involved in like migraines for example. Yep. Lots of. Lots of deep biological areas, even ADHD and schizophrenia to some degree. So the cytokines I was mentioning, like interleukin 1 and 6 and stuff, they're kind of like, adjacent to that. They're deep in. They're the deepest inflammation response in the body, really. And they're a response to fighting problems. So if you. Yeah, let's say you get some pesticide, come in. Well, it's going to create inflammation. It's like, oh, toxicity. The immune system, the body's like, fight it, fight it.

[B]

Right.

[A]

And then it creates chronic sickness at a deeper level. What ends up happening with some of these, like, chronic autoimmune diseases? Like, if you get, like, an infection, like an Epstein Barr or. Which is kind of harmless to most people, but it does cause havoc because it stays in the body a long time. It's not because it's a deadly disease because the body doesn't clear it. The spike protein, as an example. Spike protein I found interesting because it kind of like, works a bit like the glyphosate in that sense, where it causes a chronic inflammatory response, which kind of down regulates what we'd say. Down regulates the gene doesn't necessarily, like, switch them off, but turns the volume down. So you can see again how biology is a cyclical process. You might have a spike protein signal which comes out of ribosomes in the cell, the cytosol. It's not in the nucleus, so it's not. The spike protein isn't going to, like, gene areas. But what happens is it's communicating out like this signal, and then the inflammation is fighting it. And those cytokines of inflammation over time are fighting that spike protein are what can shut down gene expression. You know, so it's like it's causing the response which is causing the. The problem.

[B]

Right.

[A]

So if we have a safe and direct way of like, like going to those core genes that are shooting that inflammation and basically stop them, we would solve a lot of. We're not going to solve ALS or Alzheimer's, but we could solve a lot of chronic sickness just by simply going, you don't need to fight anymore. That's what we're doing. We're going into the body and we have to target very specific areas, and we have to basically say, stand down, soldier. Don't need to fight anymore. Because it's honestly the body fighting that is causing the sickness. We see it in Lyme's disease or in chronic diseases of all kinds.

[B]

I had that, too.

[A]

You did?

[B]

Oh, Actually, I had Lyme's disease and I took a test and I tested positive and then I changed my diet and I did all of this, this eastern medicine stuff for it and took all this stuff and did acupuncture and I got tested again and it wasn't there. And I know Lyme's disease is supposed to, it never goes away once you had it. But the amount of bacteria that was hiding within my blood was undetectable the second time I took it after fasting and doing all this stuff. So I still feel like brain fog and stuff like that from time to time. But I don't know how much of that is just natural normal memory stuff, you know, versus like actual lives.

[A]

I think I never, I never ever believe that things can't get better or go away. Yeah, I've seen it in the hardest of cases. What I will say though is that it can be very tricky. And where I go is I try to create things that can. Like in a traditional scientific format, I try to create things that can be standardized across people. You know, like our biology is so idiosyncratic and so unique to you and me that you could go in and do XYZ and it worked for you. And I go in and do it and it doesn't work for me, you know?

[B]

Right.

[A]

So like I remember, for example, spontaneous remissions happen in some one in a hundred thousand cancer patients. Right. Like there may actually be some key high consciousness moment that truly could clear, clear all disease. There was this one woman who died of stage four cancer. She had a near death experience and then she got sent back and then her cancer went away. And that's kind of interesting because usually near death experiences are, are deaths where you could bring them back. But stage four cancer, that's a weird near death experience because that means you're still coming back into a dying body.

[B]

Right.

[A]

So the cancer would then have to reverse. But it did.

[B]

Can you send me that documentation on that?

[A]

Yeah, it's a, it's a YouTube interview of this woman. I'll send it to you.

[B]

Yeah.

[A]

So spontaneous remissions do happen in some one in a hundred thousand cancer patients. But the, the point is, is that I often tell people, even though miracles do happen, we can't, we can't standardize miracles.

[B]

Right.

[A]

I, we, I'm, you know, I'm a mere mortal and I don't have the power to make miracles happen. All I have the power to do is do something that I know can work consistently and reproduce over time.

[B]

Right.

[A]

So that's what I do.

[B]

Hope is not a strategy.

[A]

No.

[B]

Right.

[A]

No. But it's not to say that there isn't like any. Each person's individual life. I do believe what we'd call miracles do happen. But. But yeah, that can't work as a, as a form. It's just like in anything. Can't run a business that way, can't run a country that way, can't cure diseases that way, even though that there are always going to be people that do somehow find the miracle. And that could be you. Unfortunately that's never been me, so I've had to do it through the hard sciences. But yeah, inflammation is a big problem and it basically works like metabolism in the sense that a dysregulated inflammatory system, like a dysregulated metabolic system, doesn't reset often on its own. It just keeps working that way until something forces a reset. And the whole structure, the way that I do molecular science is to hit multiple targets simultaneously. And simultaneous being the key. No one individual target would ever solve complex problems like this. If you had a gene therapy for autism, you would only solve 1% of autism. Most autism comes from way too many different genes. Most of it is more epigenetic than DNA level, which means it's like all of these locks in the genes that I unlocked which fixing the DNA wouldn't necessarily solve. And then of course, it's like metabolic, it's, it's ion channels, it's this, it's that, it's inflammation. So to really solve any disease, we must hit like multiple high leverage target simultaneously. And then we can, we basically are setting the conditions for the cell to return to its default baseline. And that's really the point of, of everything I'm doing in whichever area it is in. At the end of the day, I've always just been forced to have to do what my family has needed me to do.

[B]

Right. You know, do you have a job as well and something? Yeah. So in addition to all this work that you're doing and raising three kids, you also have a, a day job.

[A]

I, I have to work in between doing all this work to get, you know, obviously pay bills.

[B]

Right.

[A]

So I work in between. In between doing the first human gene reprogramming, then figuring out a functional cancer cure, then losing my wife and raising three children, two with special needs, and now having to solve every genetic disease and also build a direct consumer, nutraceutical therapy to solve inflammation and metabolism. I do also still have to work in between all of that. Yeah, yeah.

[B]

Have you ever thought like instead of a. Or in a. Instead of waiting for an investor, big investor or whatever, like some other form of like go fund me or something and to raise money to be able to continue your research?

[A]

Yes. So this direct consumer, I keep calling it a therapy, but I can't actually call it a therapy when we release it. It because otherwise that would make it, you know, something the FDA would have to approve this nutraceutical stack that we're going to give to people directly. This is going to be a fully decentralized mechanism.

[B]

Okay.

[A]

So people are going to be able to buy into it. They'll also be able to own a stake of it if they buy into it. And it's something the world can get very fast.

[B]

Okay.

[A]

So this is going to be the pathway to. To doing a. Essentially a decentralized science operation.

[B]

Tokenized.

[A]

Yeah.

[B]

Yeah. Nice.

[A]

It was other people's idea, not mine. I'm focused, you know, deeply in the scientific part of it.

[B]

Yeah.

[A]

So people close to me and people close to them kind of came together and said we're going to kind of build it this way. Do a token decentralized science. Other people, people buy in, they maybe even get some kind of form of equity or shares or whatever.

[B]

Ethereum.

[A]

Yes. Yeah, it'll be that. So then. And I don't know anything about any of that stuff at all. Like, I'm a complete boomer when it comes to crypto, so I know way too much.

[B]

I know way too much. Yeah. It has been a down cycle for a long time and I'm over it.

[A]

You know, the thing is with it though, is that I think it is that whole control aspect you can give back to people. Yeah. So this way people will be able to buy into it, own a piece and get whatever people get when they do these things because I don't know. But what I do know is that we'll be able to build it fast if we have the resources to because we don't need legal.

[B]

You're right. That's a brilliant way to do it. It's a brilliant way to set it up.

[A]

So that's going to be sort of the immediate priority while I have to do the cancer traditional through traditional paths because otherwise there's no way it's. They're ever going to let it get out to the world or however long I'll be around to even do it.

[B]

Right.

[A]

So with the cancer, I have to be super strategic and careful because I have people who ask me all the time. They're like, why are you hoarding, you know, a cure for cancer? And it's like, firstly, it's not an absolute cure. We discussed all that. But the other thing is I can't just give you chemistry and molecules because that's not legal for me to even do because I re engineered an existing drug with a doctor and a pharmacist and I can't legally pass that around to people. The other thing is I'll be killed if I do. So, you know, if we actually want this to get out to the world, it has to be done properly where we have to have stakeholders and they have their part in it too.

[B]

Right.

[A]

Because otherwise nobody gets it right. You know, so it has to be done in, you know, a strategic way. But this part we can just do straight to the world and we want to try to do that as soon as possible.

[B]

Yeah, for sure. Yeah. It's easy to do too. I mean, you can, you know, to set that up and to launch it, but. Well, that's fantastic. I mean, this has been just an incredible conversation and you've been super, you know, vulnerable and open and sharing a lot of detail and personal detail and talking through a lot of stuff that I know is a challenge to talk about and difficult to relive some of the, you know, the moments that you've been through. How can people, you know, I guess, how can people support or, you know, how can people follow you or kind of support your work at this stage prior to the tokenization?

[A]

Yeah, honestly, there's. You can follow me on X and Tick Tock and stuff like that. I, I think TikTok like banned most of my videos, so maybe X is probably the only platform that I'm kind of safe to post on. So you can follow me there. You can obviously go to ahmedbiogenetics.com but there's not really much there, I think. Look, the, the most important way it would be when we do this to, for people to come part of this decentralized project. They can actually be a part of it. They can earn shares or whatever the system is that they set up. And also they get to be part of giving the world something that's safe and effective fast.

[B]

Right.

[A]

So that would be the best way to support. Aside from that, I think just to amplify that. Look, I, I get told a lot from people, some powerful people even, many of which have reached out to me. I have supporters at top institutions. I also have people that don't like me at top institutions. I have powerful people who love me. And powerful people that hate me. And. But the. The consistent thing that I've heard a lot is that at the end of the day, the. The. Is the science might not be the most important part of this story in the end, but it might actually just be a story of how far human will can push. Because not just in Jill's case, but through everything we experienced after everything, picking up the pieces, dealing with children that, like, having another terminal clock, having disabilities, having to figure out all of this alone. It has been like being at war constantly for years and in. In, like, the hardest conditions. We talked about my story at the beginning, but, man, compared to watching Jill die, all of that stuff was a breeze. Yeah. And the only thing I can think of more terrifying than what I've already been through is what I'm gonna have to watch Aaron through if I don't succeed. And a lot of the people reach out to me and they say that they're inspired, you know, by the story as much as the science. And if there's one thing that could help us there, it's that to bring the team together. Because at the end of the day, I'm only one guy. If we're going to be able to do this, I'm going to need everyone else, too. Going to need the support, going to need the connections, going to need everything. Because this is something that affects every single person on Earth. Half the world is sick, and the other half are the family and friends of the sick. So it affects literally everybody. And the truth is, is that the human race is getting sicker. Like more children born disabled than ever. Less deaths in childbirth, certainly way less, but way more born with chronic illness than before.

[B]

Right.

[A]

More young people dying of cancer or have autoimmune diseases than ever. And of course, 20, 25% of the population is infertile, which is going to climb, too. So we are in a situation where it might not look like it right now, but if we're not successful here, two, three decades from now, the human race is going to start going off a cliff, and all of the stuff that we fought over will become meaningless because we. We. If we don't have our biology intact, we don't have anything. If we don't have our own hardware and software, what political system we have, what economic system we have, AI it's all meaningless if we don't work anymore.

[B]

Right?

[A]

And I think the most important thing is that we. We realize that sooner rather than later. Because what I'd hate to see is 10, 20 years from now, because of the, the sickness and, and the degeneration that we have gone through. Babies have to be born in, you know, gene therapy, pre. Pre embryonic gene therapy, or be born in test tubes because we're not able to do it naturally anymore, you know, and everything that we're doing in this mission, in this work is to make sure that that future doesn't happen. And, you know, I. I believe we're gonna succeed. And you can thank Jill and Aaron for that. When that, when that day comes, if I can survive long enough to get that day to come.

[B]

Love it. Love it. Well, that's powerful, man. That's. It's been amazing, you know, chatting, but I feel like that's a, that's a powerful way to kind of close out the conversation if, if, if you're good with that.

[A]

Thanks, Matt. It's been a pleasure, man.

[B]

For sure. It's been great. Yeah, You've enjoyed the experience then?

[A]

Yeah, it's been great. You have a great operation here.

[B]

Good.

[A]

It's really cool. I love the environment. I love the. All of the different things you've got going on here.

[B]

Yeah, we enjoyed hosting you and I got a lot out of this and learned a lot and want to stay in touch. Touch, too, and support your mission. So, yeah, it's been great to connect, great to get to know you, and I'm inspired and optimistic about the future. So keep doing what you're doing.

[A]

Thank you, sir.

[B]

Yep. Thank you.