In addition, CTRP9 gene knockout mice can aggravate left ventricular systolic and diastolic dysfunction, myocardial cell apoptosis, and inflammation in the ischemic heart [20], while the overexpression of CTRP9 can reduce the area of myocardial infarction after myocardial IR injury in normal or diabetic mice, and supplementing wild-type mice with the CTRP9 protein can improve cardiac function, apoptosis, and fibrosis after myocardial infarction [36, 37]. The gene discussed is C1QTNF9; the disease is myocardial infarction.