According to current research, the superoxide anion (O2•−) is largely responsible for hyperglycemia-associated endothelial dysfunction by reducing the bioavailability of the vasorelaxing and endothelium-protective factor nitric oxide (NO) via uncoupling of endothelial nitric oxide synthase (eNOS), thereby inhibiting protective mechanisms of endothelial cells and, thus, enhancing inflammatory and cell-damaging processes [12,13]. This evidence concerns the gene NOS3 and endothelial dysfunction.