FMO5 and hyperhomocysteinemia: Hyperhomocysteinemia is known to restrict NO bioavailability by influencing ROS bioavailability (through the activity of NADPH oxidase), inhibiting eNOS function (through activating protein kinase C and inhibiting the activity of the dimethylarginine dimethylaminohydrolase enzyme), inhibiting the transport of L-arginine required for NO synthesis by methylation and inhibiting the activity of glutathione peroxidase [6,11,30,32,33].