Programmed cell death is currently a critical focus in cancer therapy research. Among its various forms, ferroptosis and disulfidptosis have recently attracted considerable attention as novel mechanisms of cell death.Ferroptosis is an iron-dependent, peroxide-driven form of cell death, whereas disulfidptosis is induced by disulfide stress result ing from cystine accumulation during glucose deprivation. Both types of cell death are closely associated with tumor progression, and recent studies have demonstrated that their activation may serve as an effective strategy for cancer intervention. SLC7A11 plays a dual regulatory role in both ferroptosis and disulfidptosis, by inhibiting ferroptosis under normoglycemic conditions, while promoting disulfidptosis in glucose-deprived environments.Targeting the expression and metabolic reprogramming role of SLC7A11 and developing synergistic strategies to induce both ferroptosis and disulfidptosis may thus offer novel theoretical and clinical approaches for cancer therapy.