Inhibition of GPx4 commonly leads to cell death due to excessive lipid ROS accumulation.[53, 54] However, some cancer cells are resistant to ferroptosis even without GPx4 inhibition, indicating the existence of alternative ferroptosis defence mechanisms.[6] In this situation, FSP1 was discovered as a vital ferroptosis suppressor acting in parallel to GPx4, which facilitates the generation of CoQH2 or VKH2 by the use of NAD(P)H on the plasma membrane.[10, 11, 12] However, the posttranslational modifications of FSP1, especially ubiquitination, are still poorly understood. This evidence concerns the gene AIFM2 and cancer.