Based on the above scientific questions, we hypothesize that cardiomyocyte ADAM17 aggravates cardiomyocyte apoptosis induced by doxorubicin by regulating TRAF3–TAK1–MAPKs pathways, and inhibition of ADAM17 may ameliorate doxorubicin-induced cardiomyopathy without affecting the anti-tumor effect of doxorubicin. The gene discussed is TRAF3; the disease is cardiomyopathy.