Well, again, you're dealing with -- okay. So prior to 2015 paper, we had little if any evidence to indicate that any bat sarbecovirus was capable of replicating efficiently on the human receptor, especially in the context of a primary cell derived from the lung, the airways of a human. And so there was no data to support the idea that these were important threat viruses. After that paper, it said that there are threat viruses, followed by the WIV1 paper, that said there are threat viruses in nature, in bats, that can have the potential to cause serious human disease. We don't know for sure. A good example of this is there are strains that use the DPP4, no, let's say the ACE2 receptor of SARS coronavirus, and you put them in K18 mice that overexpress that ACE2 molecule, you can find genome equivalents but no live virus. In other words, the virus gets in, it makes a bunch of those progeny RNA molecules, but it doesn't make any progeny viruses so it can't spread. DC.Scheduling@LexitasLegal.com So the idea that just the virus receptor interaction and entry is the whole key to driving a virus to become a pandemic is just nonsense, and it's always been nonsense. In the case of coronaviruses, there are 49 genes in each of our bodies that regulate disease severity, and the person who gets really sick has a very common loci on chromosome three, with five genes on it, that we inherited from Neanderthals, according to the reports, based on people that do the sequence comparisons. And if you have that loci you're going to get really sick with sarbecoviruses.