Recently, Wang et al. reported that the transcriptional regulator PRMT4 (protein arginine methyltransferase 4), which plays a role in regulating oxidative stress and autophagy, was significantly reduced in DOX-treated cardiomyocytes.280 Interestingly, it has been found that overexpressing PRMT4 accelerated ferroptosis and worsened DOX-induced cardiomyopathy, whereas inhibiting PRMT4 activity and reducing its expression produced the opposite effect. The gene discussed is CARM1; the disease is cardiomyopathy.