> 0.3 and PHWE > 10−6. For EUR, we used genotypes at 1,318,293 HM3 SNPs (MAC > 5) from 348,501 unrelated EUR participants in the UKB as our LD reference. For EAS, we used genotypes at 1,034,263 quality-controlled (MAF > 1%, SNP missingness < 5%) HM3 SNPs from a merged panel of n = 5,875 unrelated participants from the UKB (n = 2,257) and Genetic Epidemiology Research on Aging (GERA; n = 3,618). Data from the GERA study were obtained from the database of Genotypes and Phenotypes (dbGaP; accession number: phs000788.v2.p3.c1) under project 15096. For SAS, we used genotypes at 1,222,935 HM3 SNPs (MAC > 5; SNP missingness < 5%) from 9,448 unrelated individuals. For AFR, we used genotypes at 1,007,949 quality-controlled (MAF > 1%, SNP missingness < 5%) HM3 SNPs from a merged panel of 15,847 participants from the Women’s Health Initiative (WHI; n = 7,480), and the National Heart, Lung, and Blood Institute’s Candidate Gene Association Resource (CARe56, n = 8,367). Both WHI and CARe datasets were obtained from dbGaP (accession numbers: phs000386 for WHI; CARe including phs000557.v4.p1, phs000286.v5.p1, phs000613.v1.p2, phs000284.v2.p1, phs000283.v7.p3 for ARIC, JHS, CARDIA, CFS and MESA cohorts) and processed following the protocol provided by the
