PRS were created for ASB using all available SNPs of the discovery dataset [85, 86]. PRS were computed as the weighted sum of the effect-coded alleles per individual. We calculated the PRS for subjects of five independent datasets, selected for their detailed phenotypes related to antisocial outcomes: (1) the Dunedin Study [46], (2) the E-risk study [87], (3) the Philadelphia Neurodevelopmental Cohort [88], (4) the Quebec Longitudinal Study of Child Development [89], and (5) the Quebec Newborn Twin Study [90]. All individuals were of European ancestry. To maintain uniformity across target cohorts, we adhered to the following parameters: Clumping was performed by removing markers in linkage disequilibrium, utilizing the following thresholds: maximum r2 = 0.2, window size = 500 kb. We excluded variants within regions of long-range LD [91] (including the Major Histocompatibility Complex, see Supplementary Table 16 for exact regions). Second generation PLINK [92] was employed to construct PRS for each phenotype, at the following 11 thresholds: p < 1 × 10−6, p < 1 × 10−4, p < 1 × 10−3, p < 1 × 10−2, p <
