As with most other existing GWAS of alcohol phenotypes, we are limited in power by the sample sizes for estimating genetic risk associations and thus consider our results preliminary. However, these findings provide suggestive evidence that genetic heterogeneity in the construct of AUDs/alcohol problems may exist between, and even within, different types of populations. Previous studies have identified phenotypic and genetic heterogeneity underlying alcohol phenotypes attributable to other sample-specific factors such as age of onset, patterns of symptom endorsements, and psychiatric comorbidities (Kuo et al., 2008; Dick et al., 2007; Cloninger et al., 1988; Edwards and Kendler, 2013), and so it seems that heterogeneity may be the rule rather than the exception for alcohol use disorders and other complex psychiatric and behavioral traits. This phenomenon is important to consider in light of the knowledge that heterogeneity can have major consequences on power for gene identification studies (Manchia et al., 2013), so even smaller studies such as this can provide insight into potential challenges to consider when designing large scale efforts in the future. Indeed, though gene identification efforts for alcohol-related
