Specifically, the overexpression of Metrnl in cardiac macrophages reduced in infarct size, decreased inflammatory infiltration and cardiomyocyte apoptosis, and enhanced recovery of cardiac function post-MI/RI may be that Metrnl induces M2 macrophage polarization through activation of AMPK phosphorylation. The gene discussed is METRNL; the disease is myocardial infarction.