<p>Disulfidptosis is an emerging form of regulated cell death (RCD) that is mechanistically distinct from, yet closely interconnected with, classical cell death modalities such as apoptosis, ferroptosis, and cuproptosis. It is typically triggered in cells with high expression of solute carrier family 7 member 11 (SLC7A11, also known as xCT) under glucose-deprived conditions. In this context, nicotinamide adenine dinucleotide phosphate (NADPH) becomes depleted, and consequently the level of reduced glutathione (GSH) declines, which in turn compromises the cellular capacity to efficiently resolve aberrantly accumulated intracellular disulfide bonds. As a result, disulfide stress progressively builds up and ultimately promotes abnormal crosslinking, aggregation, and functional disruption of cytoskeletal proteins, thereby driving catastrophic cytoskeletal collapse and cell death. Because SLC7A11 overexpression represents a key metabolic hallmark across multiple cancer types, disulfidptosis provides a novel conceptual framework for exploiting tumor-specific metabolic vulnerabilities. Moreover, accumulating evidence across diverse malignancies suggests that disulfidptosis contributes to tumor progression. Meanwhile, recent studies have increasingly highlighted evolving drug delivery strategies and metabolic synergistic approaches that integrate disulfidptosis with other RCD programs, and, importantly, its impact on the tumor immune microenvironment is gradually being elucidated. In this review, we systematically summarize the definition, molecular mechanisms, and biological functions of disulfidptosis, emphasize recent advances in its synergistic interplay with other cell death modalities, and discuss its implications for cancer immunotherapy. Finally, we outline emerging drug delivery strategies designed to induce disulfidptosis in tumor cells, aiming to facilitate further exploration and translational development of disulfidptosis-based anticancer therapies.</p>