We conducted a series of secondary simulations to assess the robustness of PRS-CSx in a wide range of settings: (i) varying polygenicity of the genetic architecture (0.1% vs. 1% vs. 10% of causal variants); (ii) varying cross-population genetic correlations (rg=0.4 vs. rg=0.7 vs. rg=1.0); (iii) varying sample sizes of the discovery GWAS (50K EUR + 10K non-EUR; 100K EUR + 20K non-EUR; 200K EUR + 40K non-EUR; 300K EUR + 60K non-EUR); (iv) varying ratios of the EUR vs. non-EUR GWAS sample sizes (120K EUR + 0K non-EUR; 100K EUR vs. 20K non-EUR; 80K EUR + 40K non-EUR; 60K EUR + 60K non-EUR); (v) varying SNP heritability of the simulated trait in different populations (h2=0.5 in EUR + h2=0.5 in non-EUR; h2=0.5 in EUR + h2=0.25 in non-EUR; h2=0.25 in EUR + h2=0.5 in non-EUR); (vi) varying proportions of shared causal variants across populations (100% vs. 70% vs. 40%); (vii) allele frequency and LD dependent genetic architecture: instead of sampling per-allele SNP effect sizes from a multivariate normal distribution with homogeneous variance across the genome, we assumed that the variance
