also revealed that DOX‐challenged cardiomyocytes exhibit impaired iron homeostasis, and treatment with deferoxamine or dexrazoxane inhibited myocardial ferroptosis, thereby mitigating doxorubicin‐induced cardiotoxicity.[38] Moreover, deletion of ferritin H in mice promotes cardiomyopathy ferroptosis.[52] Our experimental data revealed that EBBP overexpression confers cardio‐protection against anthracycline‐induced cardiomyocyte ferroptosis via coordinated upregulation of the SLC7A11/GPX4 axis, FTH1 expression and enhanced GSH/GSSG redox balance in both murine models and cardiomyocytes. Here, FTH1 is linked to cardiomyopathy.