Ferroptosis is a recently recognized form of regulated cell death driven by small molecules or conditions that induce lipid-based reactive oxygen species (ROS) accumulation, and this iron-dependent form of cell death is morphologically and genetically distinct from apoptosis, necroptosis, and autophagy (8,9). Ferroptosis is characterized by cell volume shrinkage and increased mitochondrial membranes and is mediated by iron-dependent lipid peroxide accumulation (10). The ferroptosis-inducing compounds, such as erastin and Ras selective lethal 3 (RSL3) could inactivate cellular glutathione (GSH)-dependent antioxidant defenses, leading to the accumulation of toxic lipid ROS (11,12). Glutathione peroxidase 4 (GPX4) is a key antioxidant enzyme that is responsible for removing lipid hydroperoxides within biological membranes (8). Once GPX4 inactivation, GSH will loses ability in removing the local peroxidase reaction, which eventually lead to a lipid ROS accumulation and ferroptosis.