Such findings are consistent with a growing body of work on the impact of interactions of specific genetic polymorphisms with specific environmental risk factors (Moffitt, Caspi, & Rutter, 2006). Emerging data from large-scale studies that measure genotypes, relevant environmental factors, and behavioral or health outcomes are indicating that identifying specific G×E interactions is possible. One of the first examples was the finding that maltreated children were more likely to develop behavioral problems if they also had a specific functional polymorphism in the gene encoding a neurotransmitter-metabolizing enzyme, monoamine oxidase A (Caspi et al., 2002). The effects of polymorphism in the promoter region for the gene encoding the serotonin receptor have also been demonstrated to contribute to G×E interactions (Caspi et al., 2003; Kaufman et al., 2004; Kendler, Kuhn, Vittum, Prescott, & Riley, 2005).
