Decreased NO bioavailability and sGC oxidation lead to inefficient sGC activation and lower cGMP output, which are associated with and directly contribute to cardiovascular diseases including ischemic heart disease, decompensated heart failure, ischemia reperfusion injury, visceral organ transplant failure, stroke, pulmonary and systemic hypertension, and atherosclerosis (Murad et al., 1978; Lucas et al., 2000; Loscalzo, 2001; Voetsch et al., 2004; Mitrovic et al., 2011). This evidence concerns the gene SGCB and atherosclerosis.