The data did not contain a sufficient number of genotyped variants that were rare in both populations to simulate rare versus common effects. Instead we examined SNPs common in both populations (common) vs. SNPs rare in at least one population (uncommon). Only common variants were used in constructing the kinship matrix, and so uncommon variants will only contribute to hg2 via LD. The common SNPs had an FSTC of 0.15, while the uncommon SNPs had an FSTC of 0.25. We simulated phenotypes with a different proportion of phenotypic variance from uncommon variants (α). When α is different from 0, the kinship matrix variant and causal variant frequencies are different. The results in Table 2 show that simulations involving a large proportion of causal variants not included in the kinship matrix (high α) had a lower value of hg2 than h2 because the common variants did not completely capture the phenotypic variance driven by the uncommon variants. The parameter α also determines the study wide FSTC according to FSTC = (0.15(1-α) + 0.25α) (see Online Methods). The results shown in Table
