The released SAS from FeA restrains the uptake of cysteine through inhibiting the pathway of glutathione peroxidase 4 (GPX4)‐cystine antiporter system Xc‐transporter (XcT) that would otherwise allow cystine to enter the cells for synthesis of GSH, leading to promoted ferroptosis.[33] As a ferroptosis inducer, Fe3O4 nanoparticles work together with SAS to synergistically initiate ferroptosis through Fenton reaction, inhibiting tumor growth. Here, GPX4 is linked to neoplasm.