Mechanically, Cao et al. found that the leakage of nucleic acids to cytoplasmic induced by ischemic myocardial injury activated the cGAS-STING signaling pathway, resulting in M1-like polarization of macrophages and the induction of inflammatory programs with increased levels of NLRP3, Caspase1, IL-1β, IL-6, IL18, TNF-α, whereas inhibition of STING or cGAS promotes the M2 transformation of recruited macrophages toward repair, which is crucial to the recovery of MI (20). The gene discussed is IL1B; the disease is myocardial infarction.