PRS performance was evaluated in an independent cohort using genotype and phenotype data for individuals of European ancestry and individuals of African ancestry (Table S1) from the UK Biobank, with imputation and quality control previously described.22 We undertook extensive post-imputation quality control of the UK Biobank, including the exclusion of relatives and ancestral outliers from within each group. Specifically, analyses were limited to self-reported European and African ancestry individuals, with additional samples excluded if genetic ancestry principal components (PCs) did not fall within 5 SDs of the self-reported population mean. For each individual, their PRS was computed as the weighted sum of the genotype estimates of effect on each phenotype from the discovery studies (Table S1), multiplied by the genotype at each variant. For each population-specific variant set, weights from either the European or African summary statistics or the fixed-effects meta-analysis were used. A total of 96 polygenic risk scores were evaluated in each phenotype exploring the impact of ancestral population (two scenarios), p value threshold (16 scenarios), and variant weighting (three scenarios). The proportion of variation explained by each
