As shown in the present study, the percentage of Ki67-labeled myocytes in the left ventricle, with diabetes and/or partial SOD2 depletion, all decreased by 50%, compared with that in C57BJ/6J control hearts, while the decrease in myocyte proliferation in hearts with diabetes and/or partial SOD2 depletion was significantly inhibited by APS treatment (Figure 2C). The gene discussed is MKI67; the disease is diabetes mellitus.