(4) IR and HINS can activate mediators of inflammation in the visceral fat, liver and muscle then impair the production and release of NO and other vasodilators [34], favor the production of endothelin-1 and the vasoconstrictive and mitogenic responses on the vascular wall [35, 36], diminish endothelium-dependent vasomotion, decrease vasodilator capacity significantly, and promote the migration and proliferation of vascular smooth muscle cells, causing atherosclerosis [37]. This evidence concerns the gene EDN1 and atherosclerosis.