The current available studies have demonstrated the protective effects of EGCG against the pathophysiological processes involved in the progress of diastolic dysfunction and HFpEF through regulation of myofibril Ca2+ sensitivity, elevation of cTnI expression, inhibition of fibril formation of amyloidogenic proteins and myocardial fibrosis, and reduction of ventricular collagen remodeling, suppression of oxidative stress damage etc. However, the clinical studies regarding EGCg applications in human patients are still limited. The gene discussed is TNNI3; the disease is Myocardial fibrosis.