Ghrelin showed cardioprotective actions in the ventricular remodeling after myocardial infarction (MI): improvement in cardiac contractility, enhancement of the antioxidant activity of the myocardium, decrease in inflammation, fibrosis, and apoptosis via multiple signaling axis: activation of Raf-1-MEK1/2-ERK1/2 and consecutive inactivation of pro-apoptotic proteins [191] and/or activation of JAK2/STAT3 and inhibition of STAT1 pathway [192]. The gene discussed is JAK2; the disease is myocardial infarction.