(Table 1) lists the 33 genetic variants that exhibited genome-wide significance and have been replicated in appropriate independent populations. The first CAD risk variant, 9p21, was published in 2007, and within 2 years, 11 more novel genetic variants were mapped showing increased risk for CAD ((12),(13),(14),(15),16). It was evident from the results of these studies that most genetic variants would have modest to minimal risk effect. The sample size to detect more of these variants would have to be greater than initially expected, which enticed most of the investigators involved in performing GWAS for CAD to pool their resources. This led to the formation of an international consortium designed CARDIoGRAM (Coronary Artery Disease Genome-wide Replication and Meta Analysis) study and involved the collaboration of 14 GWAS, each of which on its own had previously been successful (17). This brought together many disciplines and considerable expertise with a total sample size of 86,995 individuals (22,233 cases vs. 64,762 controls) of European ancestry. This involved investigators from the United Kingdom, Germany, the United States, and Canada. This consortium combined the resources of over $200 million to pursue the genetic risk responsible for CAD. Genotyping was performed with the 1 million chip array followed by imputation of over 2 million SNPs from the HapMap Project. SNPs showing a significant positive association in the Discovery population were analyzed for replication in an independent population with a sample size of 56,682. Thirteen new genetic risk variants for CAD were identified with confirmation of 10 previously identified risk variants (6). In another study involving CARDIoGRAM investigators, Reilly et al. (18) identified 2 novel variants, 1 for CAD ADAMTS7 and 1 for myocardial infarction, the ABO blood group locus. This was followed by the results from the Coronary Artery Disease (C4D) Genetics Consortium (5), which identified 4 additional risk loci related to CAD. This study also involved replication in an independent population of Caucasians and East Asians. In the same issue of Nature Genetics, Wang et al. (7) reported on the identification of a genetic variant at 6p21, which increases the risk for CAD in the Chinese population, but has no risk effect in the Caucasian population. The IBC 50K CAD Consortium, utilizing a 50K SNP array covering approximately 2,100 candidate genes, identified 3 additional novel CAD loci (19).