Contrary to previous BroadABC GWAS analyses, we did not find evidence for sex-specific genetic effects in the present study. Although we did have access to sex-specific data in considerable subsets (N = 22,322 males, N = 26,895 females), the power to detect new variants employing such sample sizes is still limited. Compared to our previous study, we found that the variance explained in independent samples by PRS based on the resulting summary statistics has substantially increased from 0.21 to 3.9%. Essentially, we found consistent links of our ASB PRS with multiple antisocial phenotypes at different developmental stages, from different reporting sources, and reflecting measurements from different disciplines (psychology, psychiatry, criminology). These links were found in individuals from New Zealand, Britain, the United States, and Canada, born as much as 30 years apart. We also show that our ASB PRS were more strongly associated with more severe and persistent types of ASB.
