Second, cardiomyocyte-specific ADAM17 knockout ameliorated doxorubicin-induced cardiac dysfunction, cardiac fibrosis and cardiomyocyte atrophy and apoptosis without compromising the anti-tumor efficacy of doxorubicin, whereas cardiomyocyte-specific ADAM17 overexpression aggravated these pathological changes in mice. Here, ADAM17 is linked to neoplasm.