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 cardiac hypertrophy.