The Cancer That Rewires Your Neurons

Added: 2026-05-05

[00:00:00]I've been pretty afraid to make this video. Cancer is an enormously heavy topic and for a long time I've had complicated thoughts and feelings about covering cancer in the same frame as these silly little cartoons. But now I think I'm ready. I think if I can make the topic interesting to you, at least some of you young future researchers might be inspired to take on this fight yourself or at least find a bit of extra motivation to continue your studies in biology. And if I can do that, I will consider this a success. In this video, we're going to talk about glyopblasto, the deadliest, most aggressive form of brain cancer. We're going to look at all the ways in which this cancer corrupts biology, how the body attempts to fight back, as well as the innovative and life-changing research that is threatening to put glyobblasto on the ropes. Fair warning, the tone of this video is likely going to be a bit more serious than my typical stuff. I'll still keep things light-hearted when I can, but I mean, it's cancer. One of the most terrifying and interesting cancers I have ever seen. But first, we need to go back to understand cancer. We need to go back to biologyy's roots. We need to talk about evolution and natural selection.

[00:01:17]Biology is beautiful. That's kind of the ethos of my whole channel. Evolution is the narrative that ultimately ties this beautiful story of biology together. As a general principle, evolution selects for biology that enables the safe passage of genetic material. By definition, if genetic material weren't good at surviving, it'd be dead. A tautology. The body evolved as a mech suit around your genetic code. Vital organs evolved to power the body. Bone evolved to protect them. Muscle evolved to better locate and acquire resources.

[00:01:50]Neurons evolved to coordinate these systems. Within these organ systems, cells are assembled and disassembled for the singular purpose of ensuring safe harbor for your passengers. The plethora of different cell types in the body all largely share the same DNA. However, they are not concerned with their own well-being. A neutrfll does not act selfishly. A neutrfil is born for a purpose to patrol the body and seek and destroy invading pathogens. A neutrfll cares so little for the passage of its own DNA that it actually uses DNA as a weapon trapping and killing pathogens.

[00:02:28]That is how strong the directive is to protect your sperm and egg. And if you're interested in learning about the immune systems premier frontline soldier, I've made a spotlight video on this incredibly interesting cell. Cancer is what happens when the overarching omnipresent directive of ensuring your passengers survive and propagate is overridden. And to understand how cancer ignores this directive, we have to understand how this directive is molecularly established. Stem cells are the baby form of all the cells of your body. Once a stem cell is born, it is given a set of instructions either from its environment or from its neighbors or from its ancestors. A stem cell born in the gut, for example, might get a set of instructions that guide it into becoming a part of the epithelium of the gut. The process by which a stem cell matures into its final form is called differentiation. Blood stem cells, for example, will become blood. But depending on the type of signal that that stem cell gets, it can also become like all of the immune system too. And the thing about differentiation is that generally this process is irreversible.

[00:03:31]This is best illustrated using the Waddington landscape idea. Stem cells are like balls that live at top a hill.

[00:03:37]There are various paths down towards differentiation, but once the ball starts rolling down, it's going to be very difficult to roll back up. And once that ball reaches the end of the hill, that ball is going to stay there. Once you're a neutrfil, you're a neutrfil.

[00:03:52]Your cell fate has been determined. Your identity has been fixed. protein stem cell transcription factors or proteins whose job it is to activate parts of the DNA that encourage stem-like behavior decrease as a cell differentiates.

[00:04:04]Meaning that the programs that govern this flexible fate are shut down. Along with that fixation of fate is a general decreased need and ability to replicate.

[00:04:14]A neutrfil does not reproduce. A neutrfil's job is to fight and die for the body. If you need more neutrfils, well, that's the job of the stem cells to provide reinforcements. And because neutrfils don't reproduce, a neutrfil is not going to experience severe selection pressure to act selfishly. A neutrfll can't propagate genetic material anyway, so it can really focus on doing the job it was programmed for. As with many things in biology, you can find exceptions to this rule about differentiation and replication, but the general principle still holds. So to sum, the job of the stem cell is to provide a self-renewing supply of specialized cells. And the job of those specialized cells is to protect the sperm and egg. They've kind of been puppet mastered by the sperm and egg to give up their own self-determination.

[00:05:02]Because terminally differentiated cells have their fates locked in and their ability to reproduce severely regulated.

[00:05:09]They function perfectly as automata that serve the hive.

[00:05:15]I mean genome. Cancer is what happens when a group of cells breaks free of this overarching directive. breaks free from the absolute control the genome has over its fate. Exactly how cancer does this is going to vary dramatically between cancers and between individuals.

[00:05:30]Speaking generally, a series of DNA damage events knocks out a couple of key genes that keep cells behaving in ways beneficial for the sperm and egg.

[00:05:38]Together, these genes are called anka genes or anti-anka genes. I have a shameful confession to make. I have always found the definition of anko versus anti- ankoa genes extremely confusing. So I will be introducing my own nomenclature for this video. Cancer genes. That's it. Genes that when they are changed from their normal form make cancer happen. Some of these genes normally encourage growth and in cancer become hyperactive and really encourage growth. Some of these genes normally stop growth and are broken in cancer.

[00:06:15]Still others normally repair DNA but when damaged allow mutations to accumulate through a combination of different broken cancer genes that were never fixed. These cancer cells break free of the matrix and begin living not in service to the genome but for their own DNA. They ignore signals to stop replicating. Instead they step on the gas pedal and proliferate. They move against the Wington landscape and become more stemlike, regaining some of their infinite potential. They grow and grow, consuming resources meant for healthy normal tissue. They grow into the precisely organized structures of the body and in the worst cases break into circulation where they can migrate to a different location and start the whole cycle all over again. In this video, we're going to focus in on glyobblastoma, a specific type of glyoma, which are cancers that originate in the ga, a family of supporting cells for the neurons in the brain. But which member of this beautiful family of GA is responsible for glyopblasto?

[00:07:17]I'm actually not sure. I started my research by going to Wikipedia. Yes, yes, I know it's Wikipedia, but Wikipedia is a really good place to start for some sanity checks. Wikipedia cites a definition given by the World Health Organization that states the origin of glyopblasto is astroitic. This makes sense given that glyopblasto cells look like astroytes. However, as I was conducting research for this video, the claim that glyobblastoma is astroitic was not really as popular as I expected.

[00:07:48]So, I followed the Wikipedia to the 2014 who report on cancer to find this curious line. Glyobblasto come in two flavors. Primary glyobblasto, which can arise denovo, which is science talk for out of nowhere, and secondary glyopblastoma, which comes from a tumor that started off as aststerytes. But hold on. In 2021, the WHO updated their patch notes and removed secondary glyobblastoma as a category entirely, reclassifying it as its own astroytoma subtype.

[00:08:21]I I hate taxonomy. Research nowadays seems to point at neuronal stem cells as the precursor to glyopblasto. This makes sense as neuronal stem cells are the most powerful stem cells in the brain.

[00:08:34]However, research indicates that any of the GLE precursors could also be fair game. Not only that, but and get a load of this, it could be astrictittes again.

[00:08:43]What? Didn't we already remove astroittes from the candidate pool? No.

[00:08:46]Take back seis. It turns out there is some evidence to show that aststerytes might be defying their programming in order to differentiate to become more stemlike, move up the weddington landscape, defying gravity, and then from that stem-like state become cleoblast. Meaning aststerytes are back in the current patch of glyopblastoma, baby. Now, why did I devote precious time in this video giving you a tour of the scientific research process instead of just telling you the answer? It's to make one thing abundantly clear. Cancer is difficult to study. A lot of confusion with the cell type origin of glyopblasto comes down to the fact that terminally differentiated mature cells are pretty easy to tell apart. But once a cell becomes cancer, they kind of backslide into some weird mushy cell fetus that can then redifferate to look like a different cell, causing a whole lot of confusion. And you can imagine that a disease where you can't even identify the cell of origin reliably is going to be pretty difficult to treat and pretty difficult to study.

[00:09:53]In the latest patch notes by the WHO, glyopblastoomas generally converge onto some shared molecular traits, including mutations in the TUR promoter, amplification of the EGFR gene, gain of chromosome 7, and loss of chromosome 10.

[00:10:08]Let's start with mutations in the tur promoter. A promoter is a region of DNA that precedes a protein coding region.

[00:10:15]The function of a promoter is to well promote the expression of a gene.

[00:10:20]Promoters contain binding sites to recruit RNA polymerase, enabling that enzyme to speed down the DNA track, reading DNA and making messenger RNA, which can then be read to make protein.

[00:10:31]In other words, in glyobblasto, the part of the DNA that enables whatever tur is to be made is broken. So what is tur?

[00:10:40]Tur is tomeorase reverse transcriptase, a component of the enzyme that elongates tieumirs. If you're at all interested in the biology of aging, you've probably heard of tieumirs before. Tieumirs are repetitive regions of non-oding DNA at the end of chromosomes. They wrap up into a knot at the end of chromosomes to prevent the tips of the chromosomes from being lost. This buffer zone is crucial for healthy aging as you can imagine that if tieamir length were to shorten, you might start accumulating actual protein gene loss at the tips of your chromosomes. In order to maintain this buffer, TUR occasionally refreshes this buffer over time. In glyobblasto, the promoter region for tur is broken, meaning the tomeorase enzyme that is supposed to be refreshing the chromosomes is being made without a crucial part. This enables a greater rate of gene loss across all chromosomes, priming the cell to start malfunctioning.

[00:11:35]Another key molecular signature in glyopblasto is amplification of the eGFR gene. Gene amplification refers to an increase of the number of copies of a certain gene. In glyobblasto, the eGFR gene can be present at a higher copy number than it's supposed to. I've talked about the process of gene duplication several times on my channel.

[00:11:54]And if you want an in-depth view on how genes can just duplicate like that, I recommend my video on gene birth linked on screen. EGFR is estimated glomelular filtration rate, which is a measure of how well your kidneys function. Whoops, sorry. Must have grabbed my notes from back when I actually wanted to be a doctor.

[00:12:17]EGFR for molecular biologists stands for epidermal growth factor receptor, a membrane protein that when bound to extracellular growth factors relays a signal to the nucleus to begin the process of growing and dividing. In glyopblastoma, this gene is found at a higher copy number, meaning glyopblastoma cells are going to be very very sensitive to signals to grow. What this means in a practical sense is that compared to their healthy neighboring cells, glyopblastoma cells are going to grow much more rapidly. One of the ways in which EGFR can be duplicated is through the expression or duplication of the chromosome that it sits on. Some glyopblastoomas might have EGFR copies duplicated on the same chromosome.

[00:12:59]Others have an extra chromosome 7 that houses EGFR.

[00:13:03]And finally, loss of chromosome 10 removes essential cancer genes, including P10, a gene that makes an enzyme that halts cell growth. You might be wondering how a cell survives chromosome duplication. In that gene birth video, I just told you that anuploloy is fatal for cells. Cancer cells, however, have those safety checkpoints that would normally cause cells to apose to survive instead.

[00:13:27]Some combination of these different molecular signatures is shared amongst cases of glyopblastoma. And it's easy to see why. Loss of functioning tomeorase increases gene loss. Duplication of EGFR increases cell growth and division. And loss of important control genes like P10 removes safeguards for cells that stop them from dividing inappropriately. With all of these limiters removed, glyopblastoma is freed from servitude to the genome and will rapidly pick up other new abilities that will make them truly, truly terrifying.

[00:14:03]On a short time scale, cancer is a statistical anomaly. Think about how many cells are actively dividing in your body right now and how rare it is for any individual one of those cells to become cancer during any given instance of cell division. There are so many different limiters placed on a cell to prevent them from becoming cancerous.

[00:14:24]But even if every cell cycle gene within the cell were to go on the fritz, the body has one final hard counter to cancer, the immune system. Believe it or not, the immune system isn't just equipped to attack foreign pathogens.

[00:14:37]The immune system has tools to kill cancer as well. Cancer cells, while genetically primed to grow rapidly, aren't immortal. They can die of natural causes. And when they do, they release special cancer antigens that macrofasages and dendritic cells can eat up, which allows them to train tea cells to seek and destroy the cancer.

[00:14:57]Cytotoxic tea cells and other immune cells flood the zone, blowing up the wouldbe tumor, releasing more antigens, starting the cancer immunity cycle all over again. Neat story, right? Except almost by definition, if you have a real cancer, this neat and tidy cycle is going to be subverted in some way. Of course, without opposition, te- cells would blow this tumor out six ways to Sunday, and you'd never have an actual cancer diagnosis. So cancers had to have evolved several tools to evade the immune system as well. There are many members of the immune system that will engage in battle with glyobblasto. I'm just going to highlight two of these stories. The first battle we will look at is between glyobblasto and the CD8 cytotoxic tea cell. A type of te- cell whose function is to blow up misbehaving cells. The effective killing range of the cytotoxic tea cell is pretty short.

[00:15:50]These cells need to make physical contact with misbehaving cells in order to deliver their cell-killing payload.

[00:15:56]But before TE-C cells can close the gap, glyobblastoma cells release extracellular vesicles that contain a horrible payload of their own. These vesicles contain a TE-C cell kill switch that shuts down and kills TE-C cells before they can even fight. What is this kill switch? TE-C cells have an important safety feature meant to prevent them from destroying the body.

[00:16:18]Programmed cell death protein one. The activator of that protein is aptly named programmed cell death protein liend.

[00:16:27]Ligant meaning binding partner. Usually this PD1L protein is used by cells to cool the jets of the immune system when their destructive power is no longer needed. The thing about cancer is that because it basically has the same code as the rest of the body, it has a complete list of exploits for every cell. Glyobblasto can make this PD1L protein too. So as TE-C cells approach they are met with a minefield of kill switches set up by the cancer. This is really bad considering cytotoxic tea cells are the premier cancer fighting immune cell. However, TE-C cells are not the only cells involved in fighting glyobblasto. In fact the most important immune cell with regards to glyopblasto is the humble macroofage. Macrofasages are known to be voracious eaters. They gobble up at pathogens and display their proteins in order to train and activate other immune cells. And while te- cells were destroyed and shut down by glyopblasto, the fate of the macrofase is actually far more disturbing.

[00:17:28]Macrofasages come in many different flavors. But there are two different types of macrofasages that come to attack glyobblasto. These are the bone-derived macrofase, the most common form of macrofase that patrols the body and the resident macrofase of the brain, the microgia. Glyobblastoma reprograms these cells by using the so-called twin cytoines CSF-1 and IL34.

[00:17:52]Both of these chemical messengers bind to the CSF1R receptor on the macrofase, which causes a shift in behavior.

[00:18:00]Instead of turning on pro-inflammatory pathways that could empower the immune system to fight, they take on an anti-inflammatory healing role instead.

[00:18:09]This rerouting of behavior causes these macrofasages to heal the tumor and tamp down any attempt at fighting in the region, physically getting in the way of other immune cells that could help out.

[00:18:21]Remember programmed at death ligant. It turns out these mind-controlled macrofasages pump out a lot more of this protein as well as other factors to really suppress TE-C cell activity providing glyobblastoma with an anti-immune shield. This wall of cells is also going to be really important for drug design as macrofasages literally cover the tumor. Not only that, but mind controlled microglea at the border of the tumor secrete metallop proteiases enzymes that help cut through the extracellular matrix. Glyobblasto can then adapt neuron-like features to escape the tumor, crawling deeper into the brain. If you thought the way glyobblastoma manipulates the immune system was terrifying, you might want to hold your breath. Glyopblasto can also rewire neurons to aid in their conquest.

[00:19:08]That's right, neurons. Cells responsible for coordinating your movement. every thought and emotion you've ever experienced, every memory you've ever had, those very same cells can be brought into the tumor micro environment to power this cancer. Glyobblasto cells form synapses with neurons and benefit from neuronal signaling to drive growth and proliferation. Neurons release brain derived neurotrophic factor that is supposed to be encouraging the growth of new neurons and synapses. These new synaptic connections that would otherwise be forming between neurons, enabling them to communicate, are now being rerouted into the tumor. When neurons fire, they release a neurotransmitter called glutamate, which binds to AMPA receptors on the other side of the syninnapse. This is supposed to enable neurons to talk to each other.

[00:19:55]But when AMPA hits the tumor, calcium rushes into the cell and turns on pathways that, you guessed it, encourage cell growth. What you have now is a uniquely horrifying situation. Even for cancer, glyobblasto rewires macrofasages and turns them against tea cells, evading destruction by the immune system. Glyobblasto also rewires neurons to feed their own insatiable hunger. I remember my reaction to reading that glyobblastoma rewires neurons and I felt such incredible despair. The idea that healthy biology could be corrupted to this extent felt sick and perverted. And yet I couldn't look away. Despite the pit forming in my stomach, I continued to read on. It is a cancer that is truly, truly fascinating. And it's that fascination that partly drives the motivation of scientists to better understand this cancer and to design better treatments that will put this cancer back into its place.

[00:20:56]So what do the good research doctors have for our cancer today? There are the triedand-true approaches of surgical removal of the tumor and radiotherapy to kill off whatever wasn't removed by surgery. Since cancer cells are already not great at repairing their DNA, giving them a targeted radioactive pulse kills them pretty handily while mostly sparing the surrounding tissue. Then chemotherapy is used to suppress any cancer cells that survived treatment. Of course, this procedure has a number of weaknesses. For one, it is invasive as any surgery is going to be. And the second weakness is that as anybody who has gone under chemotherapy can attest to, chemotherapy sucks. Not that it isn't effective, but chemotherapy's side effects are pretty hard to deal with.

[00:21:44]While this protocol can improve the quality of life for patients and prolong their good health, glyobblasto tends to bounce back despite humanity's best efforts. The 5-year survival rate for glyopblasto is just about 5%.

[00:21:58]Cancer is tedious, but the only thing more tenacious than cancer is the unbreakable pioneering human spirit.

[00:22:05]While cancer research can seem like a depressing dead end if you view success as a binary between curing cancer and not doing anything, the envelope is always being pushed with new and innovative treatments that take gradual steps towards giving people with cancer more and more years to live with the goal of having old age take them before their cancer does. In January 2025, I did a 12-hour charity live stream for glyobblasto where I got to present a few of these experiments to my live stream audience. It was in that stream that we raised enough money to reach the incentive to make this video. I do a charity science live stream every January and I'm hoping to see a few of you there. The treatment I want to share with you is one that was published just after my live stream ended. And I kid you not, this is one of the coolest drug designs I've ever seen. It started off with an innocuous question that had nothing to do with killing glyobblasma.

[00:23:02]Can researchers trace the connection glyopblastoma makes with its supporting neurons? If we can trace those connections while the cells are still alive, we might be able to better study how glyopblasto manipulates neurons. But this turned out to be a much more complicated problem than it might seem.

[00:23:19]Take a moment to think to yourself, even if you're not a molecular biologist.

[00:23:23]It's fun to have the opportunity and really work your creative muscles. Leave your comment down below. One answer might have been to take a really highowered microscope, like an electron microscope, for example, to visualize these connections. Synapses themselves are really, really tiny. And electron microscopy is how we get images like this or this.

[00:23:47]But electron microscopy can't be used for this application. EM are great for taking a snapshot of cells, but cannot be used if you want to keep your cells alive to study them. You might think to use something like a tiny needle and inject dye into the neurons that surround glyopblasto.

[00:24:04]This could work in theory, but just because a neuron is nearby doesn't mean it'll always make a connection to that cancer. And just because a neuron is far away doesn't mean it won't make a connection. The answer these researchers came to was one that I personally would have never thought of. Researchers delivered a die with the use of a modified rabies vaccine. Through the never-ending creativity of science a near perfectly lethal virus was transformed into a research tool. I'm going to describe in some amount of detail this unique modified rabies virus. If this is your first genetic circuit, you might want to rewatch this part a couple of times. I promise you if you want to experience the beauty that is engineering, it's worth it. We start off with a rabies virus that contains the gene for GFP green fluorescent protein. This means any cell infected with this virus will glow green. That's how we're going to visualize the tracing. To label all of the neurons that hook up to this glyopblast, we're going to first infect the glyopblastoma and rely on the glyopblastoma to then deliver the rabies virus to all of its connecting neurons. You might be worried that just dumping this virus on would just non-specifically target all cells in the dish. But the rabies virus the researchers chose was chosen very deliberately. This particular rabies virus is a variant that doesn't actually infect mamalian neurons. This gives researchers the ability to design a rabies that infects a cell type of their choosing. Researchers give the rabies the NVA receptor and engineer the glyopblastoma cell to express TVA, NVA's binding partner. Because the neurons don't express TVA, this rabies virus will only infect the glyopblastoma.

[00:25:49]Now our tumor in a dish has been infected by a rabies virus, forcing the tumor to make green fluorescent protein.

[00:25:56]Great. How is the rabies virus going to then trace the connecting neurons?

[00:26:00]Remember, rabies can't actually infect these neurons. the neurons don't make TVA. The solution is in the fact that glyopblasto makes synapses with neurons allowing a sneaky backdoor to enable infection. Anyway, glyobblasto packages these rabies viruses into a synaptic vesicle, the same type of packet that would contain neurotransmitters to coordinate communication between cells.

[00:26:23]While neurons can't be infected by this rabies normally, they will more than happily take up a synaptic vesicle with rabies virus Trojan horsing on the inside. Now, every neuron synaptically connected to the glyopblastoma is going to glow green. But these neurons make connections with other neurons. How do we know every neuron in the dish isn't going to light up when the infected neurons pass on this virus? This rabies virus also lacks another critical gene, the rabies glyoprotein or the rabies shell. Without it, it's not anything more than a pile of RNA. The reason why this works is because the glyobblasto was engineered to supply the rabies glyoprotein in trans or for the rabies virus. Meaning the neurons are not making rabies glyoprotein once the rabies enters the neuron. It's just there to make GFP. Again, it's a little complicated. I wouldn't mind you re-watching this bit to pump my engagement numbers a bit. But once you've understood this engineering, we can now see the payoff. This is a video time lapse of adding this engineered rabies to a dish with glyopblastoma labeled in white and magenta. Don't worry about why they're different colors. And neurons which are going to start as unlabeled and glow green when infected. The fact that we get to actually watch this neuron tracing happening live is absolutely incredible.

[00:27:47]What you're seeing here is organotypic slice culture. This is a piece of cultured brain from a human patient who needed brain matter removed for a medically necessary procedure and donated said tissue. In white and in magenta, you can see glyobblasto cells.

[00:28:02]And in green, we can see every neuron that is making a connection with those cells. And if we zoom into this box here, we can see that yes, this method does not label neurons all willy-nilly.

[00:28:14]The green neuronal processes here are connected to glyopblastoma. While the red processes are neurons that have not connected to the glyopblastoma.

[00:28:23]But this study has revealed something more than just pretty microscopy images.

[00:28:27]When glyopblasto was added to rodent brain slices, the extent of the neuronal connections glyopblasto was making was truly shocking to me. Glyobblasto wasn't just recruiting neurons nearby.

[00:28:39]glyobblastoma was making connections all the way out to the opposing brain hemisphere. This does make sense because certain neurons can get very long.

[00:28:48]Judging by this picture, you can imagine why glyobblasto is such a problem. The extent by which it can co-opt neurons is pretty intense. It makes sense that radiotherapy isn't enough to keep this cancer in check. Glyobblasto will just heal itself right back up using the neurons it controls. But what if you could with molecular precision sever each and every neuronal connection glyobblastoma had while sparing unaffected neurons? How would that even work? We know surgical removal isn't good enough without damaging nearby tissue. Do you see it? We've had the answer for the last several minutes.

[00:29:25]These researchers decided to go back to the drawing board with their modified rabies. Only this time they were going to add one more ingredient, the capsace 3 enzyme, an enzyme responsible for triggering aptosis or programmed cell death. They've engineered a way to deliver a payload only to neurons that are connected to the tumor and a way to spare all other neurons, leaving glyopblastoma alone, cold, and potentially vulnerable to a combination therapy, which of course, you know, the researchers did try. Researchers used their rabies drug alone and in combination with other drugs and found something annoyingly not straightforward. Rabies drug alone did kill quite a bit of glyobblasto, but it also doesn't really look like we're seeing synergistic effects here. Why this is, I'm not entirely sure, but what I can say is that I am excited to see this therapy is at least on par with existing known drugs for glyobblasma.

[00:30:21]Because this is a firstofits-kind approach, I'm looking forward to what else develops down this avenue. Now, I will say this treatment is far from being market viable. This was a proof of principle, but what I want to emphasize here is just how incredibly clever humanity can be. And believe me, we're going to need all of the creativity we can get when it comes to fighting cancer. Glyobblasto is the most deadly, most aggressive form of brain cancer.

[00:30:48]Patient prognosis for glyopblasto is very poor and it's a particularly tragic way to live out the last leg of your life. But for as much tragedy as glyopblasto brings, it also shines a light on how beautiful humanity is once we've decided to dedicate brilliant minds to the problem. To end off this video, I would just like to say cancer.

[00:31:17]Thank you to my YouTube and Patreon supporters. This content would not be possible without you. You are all rock stars.