We now have a reasonable framework for understanding the basic genetic architecture underlying psychiatric disease, yet the number of susceptibility loci so far identified accounts for only a small percentage of the variance in liability to disease (65). With the exception of SCZ and ASD, so few replicated loci have been identified that the need to identify more is undeniable. Still, the field is at an appropriate juncture to consider when it would be reasonable to stop looking for genes and focus entirely on studying their function. Certainly, a more complete catalog of genes and mutations would provide a clearer indication of cross-disorder overlap and disease-specific biochemical and circuit convergence. One important justification for the creation of a more complete catalog is the need to address disease heterogeneity and to understand composite genetic risk in individuals. A measure of success would be the ability to genotype individuals at known risk loci and classify their disease based on a neurobiological framework (47); this is a feasible goal for the next decade (Fig. 3). Leveraging electronic medical records, remote data gathering, and electronic media, coupled with forthcoming populationlevel clinical whole-genome studies, should accelerate these efforts.
