In our primary simulation, we randomly sampled 1% of the HapMap3 variants as causal variants. We assumed that causal variants are shared across the three populations and simulated their per-allele effect sizes using a multivariate normal distribution with the correlation between populations set to 0.7. For each population, we used a normally distributed random variable to model the non-genetic component such that the heritability was fixed at 50%. The phenotype was then generated in each population using y = Xβ + ϵ, where X was the genotype matrix, β was the simulated per-allele effect size vector in which causal variants had non-zero effects and the rest of the variants had zero effect sizes, and ϵ was the simulated non-genetic component. The simulation was repeated 20 times. GWAS was performed on 100K EUR, 20K EAS and 20K AFR discovery samples, respectively, using PLINK 1.945.
