The first results with respect to genetic and environmental contributions to the variation and longitudinal stability in childhood aggressive behaviour [39] indicated high stability and heritability of aggressive behavioural problems. Heritability was on average around 60–80% without any large gender differences in the magnitude of genetic effects. In boys, shared environment explained around 20% of the variation in aggression across all ages, while in girls its influence was absent around age 7 and only came into play at later ages. Longitudinal genetic correlations explained most of the stability of aggressive behaviour. These results are encouraging for gene-finding studies. In earlier work, the first molecular genetic evidence for aggression in childhood was reported [40]. Using genomic relationship matrix restricted maximum likelihood (GREML) analyses significant influences of common SNPs were estimated for externalising problems (SNP h2 = 0.44), for attention problems (SNP h2 = 0.37–0.71) and total problems (SNP h2 = 0.18). A previous attempt to discover genomic locations of interest for childhood and adolescent aggression (N = 18,988) identified one region in chromosome 2 (2p12) at near genome-wide significance (top SNP
