Among the numerous targets, one can distinguish Ca+2 ATPase, whose glutathionylation is a cGMP-independent mechanism of vasodilation, impaired in atherosclerosis [35]; the regulatory protein Ras is activated upon glutathionylation under the action of various atherogenic stimuli (angiotensin II, peroxynitrile, and oxidized LDL) and triggers the activation of Akt and ERK [33]. This evidence concerns the gene AKT1 and atherosclerosis.