Undoubtedly, schizophrenia (SCZ), which was subjected to GWAS meta-analysis in 36,989 cases and 113,075 controls by the PGC [(Ripke et al., 2013) for other GWAS by the PGC, see (Sullivan et al., 2017)], is amongst the most frequently analyzed and robustly associated psychiatric PRS. Using these SCZ-PRS, in Figure 2; Tables 1–6, we illustrate the utility of the PRS approach in advancing our understanding of the genetic architecture of SCZ and its relationship with other traits and disorders. Broadly, two observations are immediately apparent. First, unlike GWAS, PRS may be examined in substantially smaller samples. Sample sizes range from <200 for certain clinical traits as well as neuroimaging outcomes (e.g., brain activation during probabilistic learning task) to > 100, 000 for population-based studies of common traits, such as self-rated health; how large a sample is sufficient is addressed above in Technical Considerations. Second, effect sizes are (mostly) modest with PRS explaining <1% of the variance for correlated traits [e.g., R2 for negative symptoms in the population is 0.007, or 0.7%; (Jones et al., 2016) or 0.3% for cognitive abilities (Riglin
