In endothelial cells, hyperglycaemia has been shown to cause mitochondrial hyperpolarization and endothelial nitric oxide synthase (eNOS) uncoupling, thereby increasing reactive oxygen species (ROS) and decreasing endothelial vasodilators production as well as activating inflammatory pathways, which impairs endothelial vasodilatory capacity [1,2,3]. This evidence concerns the gene NOS3 and Hyperglycemia.