GPX4 and neoplasm: Finally, divalent iron ions oxidize lipids to produce reactive oxygen species (ROS) and promote ferroptosis.[7] Researchers have developed inhibitors against GPX4 and other ferroptosis‐inducing drugs, such as RSL3, ML210, and erastin.[8] However, due to the existence of the blood–brain barrier (BBB) and inadequate tumor vascularization, it is difficult for ferroptosis drugs to reach the tumor and maintain a therapeutic dose.[3] Most importantly, there is a compensatory mechanism against GPX4.