While BP and SCZ share much of their genetic risk loci, we now report a polygenic component that significantly distinguishes these disorders. As in previous analyses of this type (12) this polygenic component implicates a true underlying genetic architecture difference between BP and SCZ and with larger samples identification of specific loci or biologically relevant gene sets could be uncovered. In addition to the difference in contribution of disease risk from large, rare CNVs we are starting to build a knowledge base to begin to identify disease specific genetic architecture and these analyses should be expanded to include more related diseases. This kind of work could eventually provide clues in the development of molecular diagnostic tools to improve on current methods, which are purely clinical. This is especially important in the case of these SCZ and BP, which are often difficult to distinguish, especially early in the course of illness (45, 46), and in which early diagnosis and treatment could improve outcome (47).
