The overproduction of oxLDLs also seems to be essential in the development of atherosclerosis and endothelial dysfunction through several mechanisms, such as the overexpression of cell adhesion molecules (CAMs), the imbalanced activation of endothelial cells nitric oxide synthase (eNOS), and the hyper-activation of the inducible nitric oxide synthase (iNOS), which in turn enhances the inflammatory processes within the vascular intima [14–16]. Here, NOS2 is linked to endothelial dysfunction.