Since it is widely accepted that in DM there is an impairment of endothelial nitric oxide synthase (eNOS) activity as well as enhancement of production of reactive oxygen species (ROS), resulting in diminished nitric oxide (NO) bioavailability and the consequent vascular alterations [4,8], several experimental studies have focused on possible pharmacological treatment aimed to restore this alteration alone [3,9,10]. This evidence concerns the gene NOS3 and diabetes mellitus.