GPX4 and neoplasm: It exerts robust antitumor effects through three interconnected mechanisms: i) The tumor lysate coating facilitates homotypic targeting and immune evasion, thereby enhancing tumor-specific accumulation; ii) The acidic TME triggers the release of copper ions, which amplify ROS generation via Fenton-like reactions, while SOF inhibits System Xc−, thereby depleting GSH and downregulating GPX4 expression; iii) Copper ions induce the aggregation of lipoylated proteins, initiating cuproptosis, while SOF synergistically promotes lipid peroxidation, driving ferroptosis.