There are evidences showing that hyperuricemia, hyperhomocysteinemia, and increased atherogenic apoB are involved in the pathogenesis of endothelial dysfunction and atherosclerosis process by inducing proliferation of vascular smooth muscle cells, increasing thromboxane formation, impairing nitric oxide production, stimulating oxidative stress, and inducing vascular inflammation and artery damage [51–53]. The gene discussed is APOB; the disease is atherosclerosis.