Environmental factors, in particular, chronic and unpredictable stressors during childhood, are among the largest risk factors for the expression of psychopathology (Green et al., 2010). Such factors act independently and in concert with genetic liability through predisposing (i.e., gene - environment correlation, RGE) or moderating (i.e., GxE) mechanisms. PRS are beginning to be used to represent genomic liability in the context of stress. For example, five studies of depression PRS report that stressful life events or childhood trauma, as well as PRS, are independently associated with depression. However, much like the candidate single variant environment interaction literature (Duncan and Keller, 2011), these initial studies have provided conflicting evidence of their interactive effect (GxE) (Musliner et al., 2015, Mullins et al., 2016, Colodro-Conde et al., 2017). Of the 3 reports evaluating stressful life events, 2 report null interactions (Musliner et al., 2015, Mullins et al., 2016) with 1 (Colodro-Conde et al., 2017) suggesting that elevated PRS potentiates the depressogenic effects of stress. In the study with positive findings, the observed PRS x stressful life event interactions accounted for only 0.12% of
