HHcy and atherogenesis promote endothelial dysfunction by activating mechanisms of oxidative stress, including reducing bioavailability of the potent vasodilator nitric oxide (NO) [8], uncoupling endothelium nitric oxide synthase (eNOS) [9], decreasing eNOS phosphorylation and activity [10], increasing formation of damaging reactive oxygen species (e.g., nitrotyrosine and peroxynitrite) and disturbing antioxidant scavenging and buffering systems (Figure 1A,B) [11,12]. Here, NOS3 is linked to endothelial dysfunction.