Limitations of the GWAS findings should be noted. One of the significant SNPs identified (rs143244591 on chromosome 3) has little supportive evidence for association from other SNPs in the region, possibly owing to low linkage disequilibrium. However, despite stringent imputation quality thresholds for including SNPs in the analysis (r2≥0.8) and evidence of an association in the replication sample, this signal may represent an imputation artifact. Second, although none of the GWS SNPs identified in the full GWAS analysis are rare, they could be described as infrequent, with minor allele frequencies in a range sometimes associated with false-positive results (4%–6%). Also, of the GWS regions, only CSMD1 showed evidence of associations in European American and African American participants. The region containing PI4K2B, which became GWS after excluding unexposed individuals (see below), was also at least nominally associated with CAD in both populations. The 2 African American–specific SNPs were rare or monomorphic in European American participants. The lack of association in European American participants could be owing to different linkage disequilibrium patterns or the absence of causal variants. The Yale-Penn samples who
