In a mouse model of MI, the upregulation of large tumor suppressor kinase 2 has been shown to induce mitochondrial fission and the release of mtDNA, significantly enhancing the expression levels of cGAS, STING, and phosphorylated p65 in cardiomyocytes, which contribute to cardiomyocyte apoptosis (Liu et al. 2023b). This evidence concerns the gene CGAS and myocardial infarction.