It may be tempting to contrast the predictive value of PRS derived from discovery GWAS of different disorders to evaluate disorder specific or shared mechanisms that may ultimately inform nosology (e.g., do SCZ-PRS predict reward-related neural function better than depression-PRS?). We suggest that such comparisons should be interpreted with caution, for 2 reasons. First, much like recent unifactoral models of psychopathology (Lahey et al., 2012) and evidence of shared neural mechanisms (Hariri, 2009, Goodkind et al., 2015), cross-disorder GWAS (Cross-Disorder Group of the Psychiatric Genomics, 2013) suggest that common genetic variation conferring liability to various disorders may be shared. Thus, clear hypotheses are needed for expected disorder specificity which may be present for some psychiatric phenotypes, but not others. Second, the robustness of the discovery GWAS can make it challenging to compare PRS. For example, if a PRS for schizophrenia [derived from GWASs containing 36,989 cases and 113,075 controls and identifying 108 independent loci (Schizophrenia Working Group of the Psychiatric Genomics, 2014)] is associated with reward-related brain function, but a PRS derived for depression (derived from GWASs containing 9,240 cases
