On the other hand, our MR study suggests that the genetically regulated hypertriglyceridemic effects of ApoC-III may be partially associated with the increased risk for CAD, and other variants within APOC3 and/or other nearby genes in the 11q23 cluster could be contributing to the increased ApoC-III levels and effecting CAD susceptibility. This evidence concerns the gene APOC3 and coronary artery disorder.