et al., 2011; Collins et al., 2012; Lasky-Su et al., 2008). In fact, some of the findings to emerge from GWAS studies in other areas, such as Crohn’s disease, have suggested new pathways that were not previously suspected to play a role in the disorder and that drastically changed the presumed understanding of the underlying biology of the disorder (Manolio & Collins, 2009). Past experience would suggest that best guesses for candidate genes affecting environmental sensitivity (i.e., cGxE) are unlikely to fare better than they have for other phenotypes investigated to date in GWAS. The combination of low prior likelihood of a given candidate being correct, compounded by likely small effect sizes and low power for any given truly associated variant, suggests that the false discovery rate—the proportion of “discoveries” in candidate gene main effect and cGxE studies that are actually false—may be unacceptably high (Duncan & Keller, 2011).
