Silencing of XIST inhibited myocardial apoptosis in rats with MI by regulating miR-449.[47] XIST promotes cell proliferation and the expression levels of fibrosis-related proteins after MI by sponging miR-155-5p.[48] It can be seen that NEAT1, KCNQ1OT1, XIST, FCER1G, and TYROBP play key roles in the immune regulation of MI, and our findings may lead to novel insights into the pathogenesis of MI immune regulation. The gene discussed is KCNQ1OT1; the disease is myocardial infarction.