Conversely, Wang et al. [45] revealed that ER stress activation via PERK/eIF2α/ATF4 signaling protects against disulfidptosis, whereas ER stress inhibitors (e.g., GSK2656157) synergize with GLUT1 antagonists to exacerbate disulfide accumulation and tumor suppression. The gene discussed is SLC2A1; the disease is neoplasm.