Although the UKB data are derived from a single item, we observed very strong genetic correlation between MVP EA and UK Biobank REX phenotypes (rg=0.88, SE=0.07, p=8.47 ×10−34). Considering our eight GWS results in EA subjects, we observed nominal replication for five loci – TCF4 rs2123392 (beta=0.011, p=3.62×10−4), KANSL1 rs2532252 (beta=0.010, p=0.007), HSD17B11 rs7688962 (beta=−0.011, p=0.012), SRPK2 rs67529088 (beta=−0.007, p=0.03), and CAMKV rs2777888 (beta=0.007, p=0.034). Applying a more stringent Bonferroni adjustment (p<0.006), TCF4 rs2123392 survived the multiple testing correction. However, all GWS variants signals have the same direction of effect in MVP and UKB analyses (Table 1). The probability to observe concordant direction of all eight MVP-identified loci in UKB GWAS by chance is 0.4%. The whole-genome polygenic risk score (PRS) based on the MVP REX data can explain up to 0.36% (p=7.53×10−95; Figure S5) of the variance in the UKB REX item. The relatively low REX variance explained by MVP PRS in the UK Biobank cohort is consistent with the limited SNP heritability estimates for MVP and UKB REX phenotypes, 6.7% and 4.3% respectively. Since the MVP trans-ancestry meta-analysis
