 Where do I find such a fatty acid? Well, there are a couple of different alternatives. I could take a plain, saturated, stretched out fatty acid. This one is not going to work. Why? No, we don't quite know. This one, on the other hand, would work. It's the same number of carbons here. It's only here. I have six double bonds. I think we need at least three. The difference, I think, that, again, you have to trust me a bit here, is that for any type of molecule that should bind, this is actually a very flexible molecule, because you can rotate around all the bonds. If I take a very flexible molecule and move that to a very restricted state, I'm going to lose a lot of entropy. And that means that it's costly in terms of free energy. So it's not going to bind very well. This is a more rigid molecule, meaning it will not lose so much freedom when I bind it. And that's going to make the binding energy better. That's usually what we see for small, dry compounds. Sameera Yasti, who worked with us and my colleagues in Lynch-Herping, Fredrik Ansara, a few years ago, she started this with computer simulations. And in fact, she showed how these particular different fatty acids would diffuse around in a membrane. And in particular, these ones with many double bonds, they're called PUFAS. Polyunsaturated Fatty Acid. If you then take those PUFAS and throw them in a simulation where we also have this entire voltage gated ion channel, what's going to happen is beautiful. They will spontaneously diffuse and find the regions where we had that charged S4 helix. I haven't told them to, but they spontaneously end up there. Not just that, we can show that they preferentially bind to a handful of residues. And if we now take those residues and mutate them in the lab, those proteins are no longer binding PUFAS. So it appears that we have a handful of residues around this S4 helix that are responsible for the entire binding pattern. We can even create some molecular motors space on that, even if we don't have structures bound. And here do you see them in red? The red side tunes here are the ones located right next to S4 where we have polyunsaturated fatty acids bound. But if the PUFAS is bound, its negative charge is going to be placed right smack on top of this S4 helix. That should change its local electrostatic environment. And if you look at these channels, they open earlier. We shift them by, say, 10 or 20 millivolts. So it's indeed easier for the channel to open, which is exactly the effect we were after. Does that work? You bet it does. There have been clinical studies validating this. How do you eat the fatty acid? Well, this is the extra beautiful part. Normally in a clinical study, you would need lots of permissions and take this through many steps to check whether you're allowed to administer a particular drug to humans. But this is kind of a lipid. How are lipids produced? Well, our lipids are produced from fatty acids, but not in our genome or anything, but based on what we eat. And we eat fatty acids. So this is just the type of fat you eat. If we eat large amounts of unsaturated fats, in particular this type of omega-6 fatty acids or so, under certain conditions, it appears to completely obliterate the symptoms of epilepsy. This is just one form of epilepsy. I don't try this in general. There are drawbacks. You're going to need to eat a lot of these molecules. And again, eating large amounts of fat is very unhealthy, per se. But what Fredrik and colleagues in Linköping and I tried to do, and they're still working on, is that we try to find smaller molecules with the same binding properties so that they should also get the channels to open easier. But in contrast to the fatty acids, they should have orders of magnitude, higher efficiency, so that we don't have to eat so much of them. And that appears to work really well in early preclinical testing. We'll see if it turns to drugs in a decade or so.