that genetic factors influence adolescents’ selection of peers with similar temperament and drinking patterns (Fowler et al., 2007). Because genotypic factors influence susceptibility to alcoholism as well as parental monitoring and peer selection, the association between these factors may be spurious and attributable to a shared genetic liability. In addition, modest correlations were observed between genotype and parental monitoring and deviant peer affiliation, such that carriers of the G allele tended to experience lower levels of parental monitoring and affiliate with more deviant peers. In the case of our findings, causal variants need to be examined in future research while including passive gene-environment correlations (rGE) in the model, by which children inherit both genes and environment from their parents, which is particularly important with regard to our parental monitoring findings. In addition, future studies need to examine active rGE, by which children with genetically oriented tendencies to drink select a social environment in which drinking is normative or rewarded – this is especially important with regard to our findings on peer affiliation. Such associations could have important implications. For example, it may be that adolescent carriers of the G allele are more susceptible to developing an AUD when parental monitoring
