SLC7A11 overexpression is one of the most consistent features of treatment-resistant solid tumors, yet its metabolic liabilities remain therapeutically unexploited. Tumors that upregulate SLC7A11 import large quantities of cystine to fuel glutathione synthesis and resist ferroptosis, a strategy that renders them addicted to glucose-derived NADPH for disulfide reduction. Under glucose limitation, NADPH depletion causes toxic cystine accumulation, aberrant disulfide bonding of actin cytoskeletal proteins, F-actin collapse, and a distinct form of regulated cell death termed disulfidptosis. First characterized in 2023, disulfidptosis operates independently of caspases, lipid peroxidation, and reactive oxygen species, and cannot be rescued by inhibitors of apoptosis, ferroptosis, or necroptosis. Recent evidence shows that this pathway extends beyond cancer cells: intratumoral CD8+ T cells undergo SLC7A11-dependent disulfidptosis, contributing to T cell exhaustion and immune evasion. Glucose transporter inhibitors such as BAY-876 selectively trigger disulfidptosis in SLC7A11-high patient-derived xenografts while sparing SLC7A11-low tumors. Despite this, no clinical oncology framework currently stratifies patients by SLC7A11-dependent metabolic vulnerability, and no disulfidptosis-targeting agent has entered clinical trials. Challenges include the absence of validated in vivo biomarkers for disulfide stress, the dual role of SLC7A11 in both tumor survival and immune cell death, and an incomplete understanding of how tumor microenvironmental glucose availability modulates disulfidptosis thresholds. This Letter to the Editor argues that disulfidptosis is an actionable metabolic vulnerability that precision oncology has overlooked and proposes a framework for its clinical translation.