GPX4 and neoplasm: Fortunately, Fe(III)‒mediated oxidation of GSH and lipid peroxidation can directly promote tumor cell apoptosis.[8] The reduction of Fe(III) back to Fe(II) in turn triggers the cyclic Fenton reaction for generating ROS.[9] Additionally, the downregulation of defensive glutathione peroxidase 4 (GPX4) induced by GSH depleting prevents the conversion of highly toxic LOOH into low‒toxicity hydroxyl fatty acids (LOH), thus promoting the ferroptosis.