Moderate to high heritability estimates for both OD (43-50%) [10] and CD (65-78%) [11, 12] strongly suggest a genetic component to risk. Several OD risk genes have been identified through modestly-sized genome-wide association studies (GWAS) [13-16], but they have not been replicated and explain only a tiny fraction of the total trait heritability. Similarly, CD risk genes have been identified and there is evidence of genetic overlap between CD and other psychiatric disorders [17, 18], but collectively these results explain little trait heritability. Two relatively large OD GWAS papers have been published recently [Polimanti et al. [16] (4,503 OD cases) and Zhou et al. [19] (28,317 OD cases)]. These studies identified a single genome-wide significant (GWS) association for OD: a coding variant in the μ-opioid receptor gene OPRM1 (opioid receptor mu 1 gene). The sample sizes available for these studies still lag far behind those available for other complex diseases with a similar public health impact, and no large scale GWAS for CD has been performed. This problem is exacerbated by the fact that controls exposed to illicit drugs (a
