Five points are relevant for interpreting the findings across the 3 samples. First, the COMT Val/Val genotype was not associated with ADHD symptom severity (Table 1) and the association between this genotype and antisocial behavior remained after controlling for ADHD symptom severity (Cardiff cohort, b = 0.40, SE = 0.21, t = 1.91, P = .06; E-Risk cohort, b = 6.26, SE = 2.83, t = 2.21, P = .03; Dunedin cohort, b = 0.83, SE = 0.42, t = 2.00, P = .05). Second, the COMT Val/Val genotype was not associated with lower IQ scores (Table 1), and the association between this genotype and antisocial behavior remained after controlling for IQ (Cardiff cohort, b = 0.51, SE = 0.20, t = 2.55, P = .01; E-Risk cohort, b = 5.66, SE = 3.03, t = 1.87, P = .06; Dunedin cohort, b = 0.97, SE = 0.44, z = 2.19, P = .03). (Post hoc analysis also revealed no association between the COMT genotype and maternal smoking during pregnancy, a putative risk factor for conduct disorder.) Third, the association between the COMT Val/Val genotype and antisocial behavior among children with ADHD was not an artifact of ethnic stratification: The Cardiff ADHD Genetic Study enrolled only white children; our analyses of the New Zealand birth cohort (Dunedin Longitudinal Study) excluded individuals of Maori origin; and in the E-Risk Study, the relationship between genotype risk and antisocial behavior was reestimated excluding nonwhite children with ADHD (n = 15), yielding nearly identical results (b = 6.16, SE = 3.15, t = 1.96, P = .05). Fourth, the association between the COMT Val/Val genotype and antisocial behavior among children with diagnosed ADHD is unlikely to be because of selective receipt of or in response to medication. In the Cardiff clinical sample, children with the Val/Val genotype were no less likely to have ever received medication than Met carriers (χ21 = 0.06, P = .81), and among medicated children, there was no association between the Val158Met variant and positive medication response assessed by the Clinical Global Impressions scale37 (b = − 0.07, SE = 0.11, t = − 0.67, P = .51). Fifth, the molecular genetic basis for dividing children with diagnosed ADHD into those with and without risk for antisocial behavior showed some specificity to the COMT Val158Met single nucleotide polymorphism, as the association was not found with polymorphisms in 2 dopamine-system candidate genes widely hypothesized to be relevant in the pathogenesis of ADHD and its clinical features38: the 10-repeat allele of a variable number of tandem repeats in the 3′-untranslated region of the dopamine transporter gene (DAT1) and the 7-repeat allele of a variable number of tandem repeats polymorphism in the dopamine D4 receptor gene (DRD4). In contrast to COMT Val158Met, these were not consistent, significant predictors of antisocial behavior in children with ADHD across our 3 samples (Table 2).