Based on those findings, we demonstrated that CaN/NFATc3/EZH2 pathway may contribute to the process of myocardial fibrosis induced by DM, suggesting that pharmacological inhibition of CaN/NFATc3/EZH2 pathway may become an effective therapeutic strategy against myocardial fibrosis in diabetes. The gene discussed is NFATC3; the disease is Myocardial fibrosis.