Limitations of this study include the following. First, our reliance on a single genetic marker provides an incomplete picture of how GABRA2 genetic risk interacts with preventive environments across adolescence. Gene-behavior associations are likely to involve “many genes of small effect”, and our chosen GABRA2 SNP is but one small piece of the puzzle. Second, although our genetic associations appeared robust to third variables, such as ancestry and gender, we cannot conclude that the GABRA2 gene shows a causal effect on alcohol use or responsivity to intervention, as this effect may be due to GABRA2–associated behavioral traits (i.e., externalizing problems) or other genetic markers in high linkage disequilibrium with the TT genotype of GABRA2 rs279845. Third, the PROSPER project was delivered in communities of predominantly White adolescents in rural areas; it is thus unclear whether our pattern of findings would hold for adolescents of other racial/ethnic backgrounds as well as for adolescents in urban areas. Fourth, although previous findings support the validity of adolescent self-reports of drinking and drunkenness (Smith, McCarthy, & Goldman, 1995), our alcohol use measures were based
