Ferroptosis has already been validated to be an effective tumor therapeutic strategy: it is shown that a variety of oncogenes or oncogenic signals can act by regulating ferroptosis, for example, the ferroptosis activator Erastin selectively kills RAS mutant tumor cells 3; several cancer cells with specific metabolic traits, such as lipid-enriched 4, ferruginous cells 5, and specific mutations (e.g Kras, TP53 mutations 6) are susceptible to ferroptosis; moreover, drug-resistant tumor cells 7 and cells with high mesenchymal stroma exhibit a higher sensitivity to ferroptosis 8,9. This evidence concerns the gene KRAS and neoplasm.