The present study expands upon the initial AAB GWAS by Tielbeek et al.13 as well as more recently published GWAS of a behavioral disinhibition phenotype15, 16 in two important ways. First, we used a case–control sample where the cases met criteria for alcohol dependence. By virtue of the association between alcohol dependence and AAB, and the relatively high rates of individuals meeting clinical cutoffs for criterion A for ASPD in the present sample (63% of males and 24% of females) compared with American population-based prevalence estimates, it is likely that the sample was enriched for genetic variants predisposing individuals toward externalizing spectrum behaviors such as AAB. Previous work indicates that the genetic influences on AAB completely overlap with the genetic influences on alcohol dependence, other drug abuse/dependence and conduct disorder—that is, AAB does not have unique genetic influences above and beyond those shared with these other externalizing disorders.18 In view of this, gene identification efforts for AAB are likely to be more successful in more severely affected samples or in samples where participants high in AAB also tend to have
