Both genetic and environmental factors influence depression [1]. As with other psychiatric illnesses, research on the etiology of depression has identified moderate heritability estimates of 40-50% [1-6], yet recent genome-wide association studies (GWAS) have so far been unable to identify robust and replicable loci associated with depression [7]. It has been argued that some of this ‘missing heritability’ is a result of particular genes exerting an influence on risk for depression only under specific environmental conditions, or ‘gene-environment interactions (GxE) [8,9]. One of the most high profile reports of GxE involves a common functional polymorphism (5-HTTLPR) in the promoter region of the serotonin transporter gene (5-HTT). This gene encodes an integral membrane protein that transports the neurotransmitter serotonin from synaptic spaces into presynaptic neurons, which terminates the action of serotonin. The repeat length polymorphism has been shown to affect the rate of serotonin uptake [10]. Specifically, the short (S) allele of the 5-HTTLPR is associated with less transcriptional efficiency of the promoter compared to the long (L) allele [11]. Additionally, a single nucleotide substitution (rs25531, A > G) within both
