In contrast to caspase-3-induced apoptosis and receptor-interacting protein kinase 3 (RIPK3)-induced necroptosis, ferroptosis relies on unrestricted lipid peroxidation.1 High intracellular levels of ferrous ions and reactive oxygen species (ROS) are among the features that distinguish ferroptosis from other forms of cell death.2 They maintain not only the proliferation of tumor cells but also the lipid peroxidation of membrane phospholipids.3,4 Therefore, ferrous ions promote the accumulation of ROS in tumor cells through the Fenton reaction, which may have an excellent antitumor effect. The gene discussed is RIPK3; the disease is neoplasm.