That's a gain-of-function experiment. There's no other way to think about it. You can do loss18 of-function, but it doesn't prove that it's jumping across there. All you say is you knock that mutation out, it loses the ability. Gain-of-function proves it, and it's causal. So in my opinion, when I read that, that's exactly what they're asking for. They mention in there that this could involve gain-of-function research in their announcement. So part one of that grant was to do surveillance in China, looking in that case for viruses. DC.Scheduling@LexitasLegal.com As part of the thought process, there were two questions. There were two ideas that came forward. One was why don't sarbecoviruses have furin cleavage sites. And I've studied coronaviruses all my life. I know sarbecoviruses. I've seen zoonotic strains. They don't have furin cleavage sites. MERS strains do. Human coronaviruses do. Feline coronaviruses do. Why don't sarbecos? There should be sarbecos out there that have furin cleavage sites, so they were going to look for them. Once they found them and they sequenced it they were going to work on it with pseudotypes. They were going to drop those spike genes into pseudotypes and ask what's -- we were also going to look at the receptor binding domain, obviously, and I think we hypothesized in there that there should be strains with 25 percent variation in spike that could still use the ACE2 receptor. And those are obviously of interest because if you're interested in developing pan18 sarbecovirus vaccines or drugs you want, in essence, the bookends of the heterogeneity that exists in the virus subgenus, right. You want strains that you know and strains that are very different, because you have no idea what would emerge in the future. So if you have breadth then you have a better chance of developing something that could be used immediately. So those are two major features. The first part would DC.Scheduling@LexitasLegal.com be then to find sarbecoviruses. If we found the sarbecovirus with a furin cleavage site it would be dropped into a pseudovirus, and its biological characteristics evaluated by the Chinese. They would remove the furin cleavage site. They would introduce changes into the receptor binding domain and look in the context of those pseudotypes, which is the safe system, to ask questions about what the role of those mutations were in tropism and entry of viruses in receptor usage. Following gleaning that data, we would then use a zoonotic sarbecovirus as a receptacle to drop the spike genes of some of these viruses, and if we found one with full-on furin site we would put it in there and evaluate its biology. We would also remove that furin cleavage site and ask what the effect was on pathogenesis in replication. So it's a loss-of-function first. At the end of that there was speculation that if the furin cleavage site looked like it was having effect on replication of pathogenesis we would consider putting it into a gain-of-function scenario where we would drop it into a null backbone. So that's how the experiment was written.