Decreased bioavailability of nitric oxide (NO), resulted from decreased synthesis of NO, reduced activation of endothelial nitric oxide synthase (eNOS) or increased quenching of NO by reactive oxygen species (ROS) [5], is believed to be one of the major determinants of microvascular endothelial dysfunction in aging, hypertension, diabetes, hyperlipidemia, and smoking [6–9]. Here, NOS3 is linked to endothelial dysfunction.