Several mechanisms contribute to the genesis of endothelial dysfunction, such as the reduced activity of endothelial NOS (eNOS) enzyme and, therefore, NO production, increased levels of reactive oxygen species (ROS) and pro-inflammatory cytokines (IL 1, TNFα), increased vascular permeability, increased vascular stiffness, and inability to regenerate from endothelial progenitor cells (EPC) [23]. The gene discussed is NOS3; the disease is endothelial dysfunction.