Excessive ROS and oxidative stress (likely arising from both increased ROS generation from NADPH oxidase, MPO and iron, and decreased antioxidant systems from PON1 or catalase, among others), play an important role in the initial phases of the disease by inducing endothelial dysfunction (i.e., impaired NO-dependent vasodilation and increased endothelial activation) and by facilitating oxidation of LDL and HDL. The gene discussed is FMO5; the disease is endothelial dysfunction.