fit to the observed results is poor for EAs (R2 = 0.07, P = 0.68 for 5,000 causal loci), with the genome-wide scores explaining substantially less of the variation in the disease phenotypes. For AAs the signals are more concordant; however they also are noticeably attenuated relative to those obtained for rare/uncommon risk alleles, with the model based on 1,000 causal loci fitting best to the observed R2 values (R2 = 0.79, P = 0.044). In addition to these six models, we also tested mixed models representing rare and common causal loci drawn randomly from the MAF spectrum. As one would expect, the simulated R2 profiles are intermediate to those reported for the models discussed above (Fig. S5), with the ones based on 100 and 5,000 causal loci fitting best to the observed results for AAs (R2 = 0.80, P = 0.04) and EAs (R2 = 0.38, P = 0.27), respectively.
