We previously reported that the heart tissue SOD activity was compensatorily increased, but both the plasma and heart tissue levels of free 15-F2t-isoprostanes were still increased in diabetic rats at the early stage of 4-week diabetes [6], which indicates that, during early stage of diabetes, compensatory increase in myocardial SOD was not sufficient to combat hyperglycemia-induced oxidative stress. The gene discussed is SOD1; the disease is diabetes mellitus.