NOS2 and myocardial infarction: In addition to mtDNA leakage and ER stress, researchers found in mouse models of myocardial infarction that the expression of some key inflammatory substances (e.g., inducible nitric oxide synthase; iNOS) was reduced in the absence of cGAS and STING and could contribute to the conversion of macrophages to a repair phenotype, which improved the survival of myocardial infarction mice [25, 95].