Some mechanisms of these impairments in diabetes may include factors that decrease endothelium derived relaxation factors such as reduced conversion of arginine to NO (19), increase in nitric oxide synthase (NOS) inhibitor (20), reduced NOS cofactor tetrahydrobiopterin bioavailability (21), and increase in endothelium derived relaxing factor (EDRF) destruction by oxidative stress (22), increase in endothelium-derived constricting factors (23, 24), endothelial cell apoptosis (25), and impairment of smooth muscle cell function (26). This evidence concerns the gene AHSP and diabetes mellitus.