Both invitro and in vivo evidence suggest a correlation between statin therapyand reduced expression of metalloproteinases and proteolytic enzymes, whoseupregulation promotes inflammation, leading to smooth muscle apoptosis [42].Furthermore, statins effectively ameliorate endothelial dysfunction throughpleiotropic actions, including increasing the expression of endothelial nitricoxide synthase (eNOS), promoting nitric oxide production, inhibiting Rhoprenylation, and exerting antioxidant and anti-inflammatory effects [43, 44]. The gene discussed is NOS3; the disease is endothelial dysfunction.