Recently, Luo et al. (88) found that high glucose induces ferroptosis in human umbilical vein endothelial cells (HUVECs) and concluded that ferroptosis is involved in endothelial dysfunction via p53-xCT (the substrate-specific subunit of system xc−)–GSH axis, suggesting that ferroptosis might participate in the process of DCM. The gene discussed is SLC7A11; the disease is endothelial dysfunction.