Aberrant cGAS‐STING activation has been observed in cardiovascular disease models[41] including ischemic myocardial infarction,[42, 43] cardiac hypertrophy,[44, 45] chronic kidney failure induced heart failure[46] and in cardiac endothelial cells in doxorubicin induced cardiotoxicity.[47] Contrary to the notion of blocking myocardial apoptosis by using BAX and BAK inhibitors,[48, 49] our results propose a model where doxorubicin drives mPTP opening (BAX, BAK, and VDAC) and releases mtDNA into the cytoplasm which triggers cGAS‐STING activation. This evidence concerns the gene CGAS and chronic renal failure syndrome.