In another study that the mice underwent permanent CAO[26], myocardial infarction promoted cardiac contractile dysfunction, and left ventricular myocardial fibrosis, and increased the amount of NLRP3, cleaved caspase-1, cleaved IL-1β, cleaved IL-18 in left ventricular tissue for four weeks. The gene discussed is NLRP3; the disease is myocardial infarction.