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 architecture supporting the development of psychopathology (e.g., depression) in the context of stress may be distinct from the genetic architecture conferring general disorder risk as assessed in the original GWAS from which PRS were derived.
