Gene silencing of p66(Shc) has been proven to restore endothelium-dependent vasorelaxation, counteracting cell apoptosis by preventing cytochrome c release, caspase 3 activity, and cleavage of poly (ADP-ribose) polymerase in vitro and in vivo, suggesting p66(Shc) as a potential therapeutic target in endothelial dysfunction [48]. Here, SHC1 is linked to endothelial dysfunction.