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 variance in depression; however, their estimates suggest that it could potentially account for as much as 20% of variance in depression if PRS were derived from a larger GWAS. While significant PRS interactions with childhood trauma explained up to 1.9% of variance in depression, the shape of these interactions was inconsistent. One study found that childhood trauma was associated with increased depression risk among those with lower polygenic liability to depression while depression PRS were associated with elevated depression risk in the context of no childhood trauma (Mullins et al., 2016). In opposition to these findings, the other report found a significant interaction wherein elevated PRS was associated with increased childhood trauma-related depression (Peyrot et al., 2014). Multiple explanations may be evoked to explain these discrepancies such as the use of PRS derived from different GWAS and differences in phenotypic assessments, and sample composition and size. GWAS x E studies are needed (e.g., (Polimanti et al., 2017) as the genetic
