ACSL4 and neoplasm: Inactivation of NF2, a tumor suppressor, rendered cancer cells more sensitive to ferroptosis by NF2-YAP axis through upregulating the expression of transferrin receptor (TFRC) and acyl-CoA synthetase long-chain family member 4 (ACSL4) [18], while genetic inhibition of the iron metabolism key regulator (IREB2) causes tumor cells resistant to ferroptosis [1].