For instance, tumor cells were capable of removing the lipid ROS via FSP1–CoQ10–NAD(P)H pathway in a non‐GPX4‐dependent manner, which may act in parallel with the GSH‐dependent antioxidative defense to prevent ferroptosis.[20, 21] In another study by Jiang et al., the authors discovered that immortalized MCF10A cells showed upregulated Prominin2 expression under pro‐ferroptotic stimuli, which is a pentaspanin protein capable of promoting the formation and secretion of ferritin‐containing multivesicular bodies and exosomes. This evidence concerns the gene GPX4 and neoplasm.