These findings converge with broader models of doxorubicin-induced cardiomyopathy, in which ROS overproduction, NF-κB and MAPK activation, and TGF-β1-driven myofibroblast differentiation contribute to interstitial collagen deposition, ventricular stiffening, and eventual heart failure [49]. This evidence concerns the gene TGFB1 and heart failure.