Recently, animal experiments have demonstrated UA reduces endothelial nitric oxide synthase (eNOS) activity as well as nitric oxide (NO) amounts by inducing mitochondrial calcium overload, endoplasmic reticulum (ER) stress and xanthine oxidase activation in human umbilical vein endothelial cells (HUVECs), which results in apoptosis and endothelial dysfunction [6–8]. The gene discussed is NOS3; the disease is endothelial dysfunction.