Overexpression of let-7i inhibits cardiomyocyte proliferation, whereas the suppression of let-7i induces cardiomyocyte proliferation and improves cardiac function in response to MI by enhancing E2F Transcription Factor 2 (E2F2) and Cyclin D2 (Hu et al., 2019). The gene discussed is E2F2; the disease is myocardial infarction.