Whereas, APR-246 can also induce p53-independent cell death, Birsen and et al. [171] demonstrated that AML cell death occurring early after APR-246 exposure is suppressed by iron chelators, lipophilic antioxidants and inhibitors of lipid peroxidation, correlating with the accumulation of markers of lipid peroxidation, consequently, the cytotoxicity of APR-246 is exerted in a ferroptotic way. Here, TP53 is linked to acute myeloid leukemia.