 So, the two studies that are going to be published in Nature talk about the whole thousand genomes project and what was found. So the two papers, one is kind of an overall paper focusing on all the variation. The other one is specifically focused on the structural variation. Looking at 2504 people from 26 populations, there were 88 million sites in the genome where people were found to differ. So that's a lot of genetic variation. Most of those variants are rare, but about 12 million of them are found at more than 5% frequency. This includes samples from East Asia, such as Japan and China, samples from South Asia, such as Bengali and Tamil, samples from Africa, including the Yoruba and Isan, samples from Europe, I should say ancestry from Europe, including people from Utah and the Finns, and samples from the Americas, including Mexican Americans, people from Barbados, African Caribbean ancestry. An interesting thing that was found in these studies is that most genetic variation is common to all populations. Things like apiobloid types, Alzheimer's risk variants, the ApoE variants, they're in all populations, so most of the variation from person to person. You could be an Isan population in Nigeria, and have one person to another has these variants, or you could be a Fin, or you could be Han Chinese, and you still have apiobloid types, for instance. So most variation among people really is shared, which is different from what, just based on what people look like, you say, oh, people in different populations must be very genetically distinct. That's really not true. The differences are not very large. Another result from these studies, it turns out when people have done genome-wide association studies, most of the variants that contribute to risk of disease are not in genes. So clearly they're in regions that are regulatory for genes that affect how genes are turned on or off or how they operate, but they're not just genes. So there's a lot of focus on genes, but it's really important to broaden that, to recognize that the way we function is not just the genes themselves, but what regulates how the genes work. So a lot more functional work is needed to really be able to interpret someone's genome. We're talking about personal genomics. If you have your genome sequenced, so here's a CD, here's your genome. What does it mean? At the moment, we actually have very little idea, certainly for certain diseases, mostly rare diseases. We have a very good idea. If you have this variant, you're going to get that disease. But mostly for the common diseases, for the complex diseases, type 2 diabetes, depression, asthma, heart disease, all these diseases, there's a very complex interaction between a whole bunch of genetic variants and the environment. And so it's not just, you have this variant, you get this disease. And yet, these are very common diseases, there is a genetic contribution, we can understand that better. We can hopefully develop ways of preventing the disease, treating the disease. And so in order to have a better understanding of that biology, we really need to have a better understanding of how those variants work to increase the risk. So it'll be very, very important to get functional studies to go from the black box of the variants to people having disease. When the paper comes out, it sounds like, okay, the project's over, what are you going to do next? When I finished HATMAP, which was a precursor project to this, people were asking me, did I still have a job? What happens is that you keep on moving. Part of our job as program officers is to be considering what the next projects are. Already, I've been involved in a functional variation RFA to try to understand what are the causal, to try to support researchers to develop approaches to figure out which are the causal variants. I work with Aaron Ramos for ClinVar, which is a database of phenotypic and clinically significant variants. And so in thinking about function, thinking about all of the variants. So I've already been moving on, trying to anticipate what's needed next. Our job is to create the future.