In endothelial cells, insulin resistance can reduce the tyrosine phosphorylation of IRS-1 and IRS-2, decrease the activity of the PI3 K-Akt signaling pathway, and subsequently affect the activity of nitric oxide synthase and the release of nitric oxide, ultimately leading to endothelial dysfunction, decreased vasodilation capacity, and the promotion of arterial plaque formation and atherosclerosis in coronary disease patients[30, 31]. This evidence concerns the gene IRS1 and coronary artery disorder.