Population, screening, and case ascertainment differences between datasets led to the assumption that there would be substantial cross-dataset variation in PTSD genetic signal. We investigated this possibility using the software MiXeR22,23. Overall, we found no evidence for subset-specific genetic causal variation (see Supplementary Note, Supplementary Tables 3 and 4 and Extended Data Fig. 1 for further details). Given the similarities of the PTSD subsets, we performed a sample-size weighted fixed-effects meta-analysis of GWAS. For the EA meta-analysis (137,136 cases and 1,085,746 controls), the GC lambda was 1.55, the LDSC24 intercept was 1.0524 (s.e. = 0.0097) (Supplementary Table 5), and the attenuation ratio was 0.0729 (s.e. = 0.0134), indicating that 92.7% of the observed inflation in test-statistics was due to polygenic signal; thus, artifacts produced only minimal inflation.
