Although stable overexpression of SOD2 in RINm5F and INS-1E cells provided complete protection against cytotoxicity by conferring resistance to oxidative stress damage [57, 58], the use of exogenous antioxidant supplementation in the majority of antioxidant clinical trials has demonstrated limited success and failed to show significant advantages in the prevention among subjects with or without clinical sign of cardiovascular complications [59]. The gene discussed is SOD2; the disease is complication.