In a DOX-induced cardiomyopathy model, knocking down TRIM21 upregulated the p62-KEAP1-Nrf2 antioxidant pathway, alleviating both DOX-induced mitochondrial deformation and elevated lipid peroxidation levels in cardiomyocytes.443 This suggests that TRIM21 plays a role in promoting ferroptosis and cardiotoxicity. This evidence concerns the gene NFE2L2 and cardiomyopathy.