For example, genes, such as the KLF2/PLPP3 axis, inhibitor of DNA binding-1 (ID1), heme oxygenase 1 (HMOX1), and nitric oxide synthase 3 (NOS3) may play hemodynamic-related roles in the development of CAVD by regulating other procalcification genes, such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) [39], by promoting endothelial repair [40] and by protecting against OS and atherosclerosis [37]. The gene discussed is NOS3; the disease is congenital bilateral aplasia of vas deferens from CFTR mutation.