GPX4 and cancer: Ferroptosis is governed by the cyst(e)ine/GSH/GPX4 antioxidant axis, which is fueled by NADPH.[23] The decrease of NADPH may be a biomarker predicting for ferroptosis sensitivity,[10] and depletion of NADPH directly sensitizes cancer cells to ferroptosis, further supporting NADPH as an important propellant for the ferroptosis defense system.[24] However, NADPH may be a double‐edged sword in ferroptosis regulation, since it is also a substrate for NOXs.