 Let me show you an example of a biological. This is a small peptide called GLP1, glucagon-like peptide 1. We don't have a whole lot of creativity in this field. Sorry about that. This is a peptide that binds to the glucagon receptor, the GLP1 receptor, which is actually a GPCR, and you know the GPCRs by now. This particular peptide, when it activates this receptor, it leads to insulin release and a decrease in glucagon. And this means that we can use this to potentially treat diabetes of type 2. There is a company in Scandinavia that is the world specialist in this, Novo Nordisk in Copenhagen. And they have worked on this type of proteins for a very long time. I won't go through the entire process here, but on the one hand, this is a process that works great, even with the peptide. The problem with the peptide itself only has a 30-minute half-life in the bloodstream. And that leads to tons of complications where you need to have a slow and steady release. You would almost need an injection needle and constantly pump something into it. It would be much better if we could have a drug that was slowly released over 10 hours or so. So you only needed one injection per day, because again, injection is required. What Novo Nordisk did is that they created a new drug called lyraglutide. And this lyraglutide had the fatty acid merged to the protein, covalently bound to the protein in the middle of it. So this is a relatively small fatty acid, but it's also a relatively small protein. What this apparently does to the protein is that it almost causes them to aggregate. This fatty acid is, let's say, they're hydrophobic, but it's not just that the fatty acids are aggregating with each other. This hydrophobicity apparently causes them to bind to albumin in the bloodstream, another protein, and that creates a very large aggregate. That might sound bad, but it's awesome, because these aggregates means that they're now bound together and they're not going to be active in this form. But eventually over 10 hours or so, these aggregates tend to release and then they bind to the receptor. So this small fatty acid bound creates this slow and steady release over 10 hours. This particular drug is marketed on the name Victoza. It's on the market and Novo Nordisk is likely making a lot of money for it. And the reason I bring this up is that Magnus Andersson, who used to be in our team before, but now a professor in Umeo, he spent about two years with Novo Nordisk doing molecular dynamic simulations and neutron scattering experiments because they had no idea what the actual structure of this complex was and what happens when the proteins were released from each other. But just to give you an example that these seemingly minor properties that what is the kinetic barrier if a molecule is releasing from another drug, it might seem like a minor detail in biophysics. But to these patients, it's the difference between needing an injection every 30 minutes or every 12 hours, which is super important for health. But it's of course also a very profitable market for Novo Nordisk.