Utilizing both CLP-induced sepsis myocardial injury models and LPS-induced cardiomyocyte sepsis models, Liu et al. demonstrated that Ginsenoside Rg1 could suppress the pro-apoptotic protein Bax, activate Akt, induce GSK-3β phosphorylation, inhibit apoptosis, and restore mitochondrial calcium homeostasis in cardiomyocytes, thereby ameliorates cardiac function in septic mice 195. The gene discussed is BAX; the disease is Sepsis.