These effects, which are ultimately anti-atherogenic, include induction of the endothelial nitric oxide synthase (eNOS)/NO pathway and result in an increase in NO bioavailability, suppression of endothelial ROS production following exposure to deleterious stimuli, such as hyperglycemia or high free fatty acids (FFAs), and modulation of vascular tone (see review [16]). The gene discussed is NOS3; the disease is Hyperglycemia.