Our study demonstrated that mitochondrial oxidative damage and the escape of mtDNA into the cytosol caused by FFA-induced lipotoxicity could trigger the activation of the cGAS-STING pathway, which switches on the initiation of NLRP3 inflammasome-dependent pyroptosis and the proinflammatory response, hence promoting myocardial hypertrophy during the progression of DCM. The gene discussed is STING1; the disease is familial dilated cardiomyopathy.