Our genetic correlation analyses confirmed previously reported [16, 23, 58] correlations between ASB and a wide range of traits and diagnoses. The relatively small GWAS sample size of some traits, however, coupled with wide confidence intervals (such as agreeableness, rg = −0,81, s.e. = 0.47) calls for larger samples in order to achieve more precise estimates concerning the genetic overlap between personality and ASB. It seems worthwhile to mention again here that partially overlapping genetic architectures do not provide causal insights of any kind. In this case they merely signify the presence of some potentially shared biological mechanisms linking the conditions [59]. One can reasonably conclude, though, there are likely common underlying genetic factors which operate to increase a general vulnerability to a range of psychopathologies. These comorbid effects are in line with findings in the Dunedin Study demonstrating that life-course-persistent offenders are characterized by several pathological risk factors, related to domains of parenting, neurocognitive development, and temperament [52]. This signifies the importance of investigating pleiotropy and considering the complex etiology of the broader ASB phenotype. Large-scale collaborations, such as
