Termed multifinality in developmental psychopathology, similar adverse experiences produce a variety of outcomes; for example, while some individuals develop anxiety and depression, others develop conduct problems, and many exhibit comorbidity (Cicchetti and Rogosch, 1996). Numerous factors likely contribute to these individual differences, including one potential source of variation: genetics. While we recognize that evocative effects of genes might contribute to child behaviors that elicit more adverse parent behavior (O'Connor et al., 1998), more relevant to this discussion is exploration of the moderating effects of several candidate genes on the impact of ELS. Of particular relevance is the increasing evidence that the serotonin system plays a critical role. Individuals who are either heterozygous or homozygous for the short form of the 5’ promoter region polymorphism (SLC6A4) in the serotonin transporter (SERT) gene might be particularly vulnerable to ELS/early maltreatment. In humans, the short SERT allele is associated with increased risk of early onset depression in response to maltreatment in childhood (Caspi et al., 2003) thus demonstrating a gene by ELS interaction. In Rhesus monkeys, Bennett et al. (2002) showed that animals
