TP53 and neoplasm: In the ferroptosis model induced by RM, various small molecule inhibitors (ferrostatin-1 and ferrostatin) to prevent lipid peroxidation could effectively inhibit cell necrosis induced by hydroxyquinoline and ammonium ferrous sulfate.[13] Although the conventional activities of p53 such as cell cycle arrest, senescence, and apoptosis are well accepted as the major checkpoints in stress responses, accumulating evidence implicates the importance of other tumor suppression mechanisms.