and thus increase α level, which may be able to detect some novel risk loci missed in previous studies due to too conservative Bonferroni correction. Fourth, we completely separated EAs and AAs in the analysis to increase the population homogeneity, and controlled for admixture effects in the association tests. Fifth, we used EAs and Australians as replication samples, and then used different samples with distinct ethnicity to detect eQTL signals, as a confirmation of variant functions to the discovery association findings. Although using distinct samples in one study might increase the false negative rates due to sample heterogeneity, replication in distinct samples does make the false positive findings less likely. Replicable findings in distinct populations would be more generalizable to more other populations, and would be more likely to appear on the causal variants. Sixth, we applied innovative definition of replication. The primary target of investigation in the current study was not the top-ranked SNPs in the discovery sample as previous GWASs, but rather the replicable risk regions. This idea was similar to that in a prior study [4]. In the replicable risk regions, there should be not only many individual markers replicable between the discovery and replication samples, but
