Historically, molecular genetic research on AAB has been limited to the examination of a small number of candidate genes with purported biological relevance; only recently have researchers begun to conduct atheoretical genome-wide scans for this phenotype.13, 15, 16 In our genome-wide investigation, we found that autosomal SNPs accounted for ~25% of the variation in a dimensional measure of AAB. Although this estimate was not statistically significant (P=0.09), which is likely attributable to our modest sample size, it maps nicely to meta-analytic findings that additive genetic influences account for 32% of the variation in antisocial behavior.7 Our finding also maps to recent GCTA analyses in a community-based sample, where it was found that common genetic variation accounted for 26% (P=0.002) of the variation in a behavioral disinhibition phenotype.16
