GWAS analysis was carried out by logistic (for the two binary traits) or linear (for the quantitative traits) regression for each ancestry group and tranche using PLINK 2.024 on dosage data, covarying for age, sex, and the first 10 PCs. Meta-analysis was performed using METAL25. We applied a standard genome-wide multiple testing correction (P < 5 × 10−8). No additional multiple testing correction was applied with respect to the number of phenotypes tested due to their high genetic correlation (rg > 0.9). The association results were populated and visualized using Phenogram79. The risk loci were enumerated using FUMA80, and each locus containing more than 10 SNPs was fine-mapped using CADD28 and CAVIAR27 for PCL-Total in the EUR population only as no significant associations were observed in the AFR population, and EHR case-control phenotypes for both populations. To understand the biological effect of SNPs associated with PTSD phenotypes, we analyzed top SNPs (at suggestive threshold P < 5 × 10−6) for their unique and overlapping distribution across the five phenotypes. The top SNPs for each phenotype were LD pruned (r2 =
