Both in mice with acute myocardial infarction and in neonatal murine cardiomyocytes treated with hydrogen peroxide (H2O2), the expression of SOX4 was markedly increased, and overexpression of SOX4 induced cardiomyocyte apoptosis with or without H2O2, whereas knockdown of Sox4 could alleviate H2O2-induced myocardial apoptosis [93]. The gene discussed is SOX4; the disease is acute myocardial infarction.