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Insulin resistance, chronic inflammation, and aberrant activation of the KRAS\u2013mTORC1 signaling axis collectively foster a tumor\u2010permissive microenvironment and disrupt glucose regulation. Recent advances have highlighted disulfidptosis, a novel NADPH\u2010depletion and disulfide\u2010accumulation\u2013driven cell death, as a therapeutic vulnerability in KRAS\u2010mutated, cystine\u2010dependent tumors. This process is linked to the metabolic interplay between glutamate\/glutamine and cystine\/cysteine, intersecting with mTORC1 signaling and GPX4 regulation. Key regulators, including system Xc\n                    <jats:sup>\u2212<\/jats:sup>\n                    , GPX4, and GLUT, orchestrate the interplay between insulin resistance, redox imbalance, and oncogenic signaling in T2DM\u2010associated pancreatic cancer. High expression of cystine\/glutamate antiporters (system Xc\n                    <jats:sup>\u2212<\/jats:sup>\n                    ) promotes cystine accumulation and NADPH depletion, sensitizing tumor cells to disulfidptosis under glucose deprivation. Biomarker\u2010guided precision medicine approaches leverage SLC7A11, GPX4, and p\u2010mTOR expression to identify patient subsets vulnerable to dual metabolic\u2013redox disruption. Emerging therapeutic strategies focus on restricting glucose availability or manipulating antiporters to induce disulfide stress. Integration of metabolic inhibitors with immune checkpoint inhibitors induces immunogenic cell death and overcomes the immunosuppressive pancreatic tumor microenvironment. Targeting these pathways may overcome therapy resistance and improve outcomes in KRAS\u2010 or mTOR\u2010driven malignancies. This review synthesizes mechanistic and translational insights into the cyst(e)ine\u2013mTORC1\u2013GPX4 axis, glutaminolysis, biomarker\u2010guided precision medicine, and disulfidptosis, offering a foundation for future therapeutic development in T2DM\u2010associated pancreatic cancer.\n                  <\/jats:p>","DOI":"10.1002\/cbf.70249","type":"journal-article","created":{"date-parts":[[2026,7,2]],"date-time":"2026-07-02T09:16:47Z","timestamp":1782983807000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Redox Metabolism and Metabolic Vulnerabilities in Diabetes\u2010Driven Pancreatic Cancer: Targeting System Xc\n                    <sup>\u2212<\/sup>\n                    , mTORC1, and Disulfidptosis as Therapeutic Strategy"],"prefix":"10.1002","volume":"44","author":[{"given":"Francis Jegan","family":"Raj","sequence":"first","affiliation":[{"name":"Bioprospecting Laboratory, Department of Botany Bharathiar University Coimbatore Tamil Nadu India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anish Ruban","family":"Solomonraj","sequence":"additional","affiliation":[{"name":"Bioprospecting Laboratory, Department of Botany Bharathiar University Coimbatore Tamil Nadu India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5874-8949","authenticated-orcid":false,"given":"Parimelazhagan","family":"Thangaraj","sequence":"additional","affiliation":[{"name":"Bioprospecting Laboratory, Department of Botany Bharathiar University Coimbatore Tamil Nadu India"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,7,2]]},"reference":[{"key":"e_1_2_23_2_1","doi-asserted-by":"publisher","DOI":"10.2337\/DB22-0942"},{"key":"e_1_2_23_3_1","doi-asserted-by":"publisher","DOI":"10.2174\/156652412803833553"},{"key":"e_1_2_23_4_1","doi-asserted-by":"publisher","DOI":"10.1007\/S00125-002-1009-0"},{"key":"e_1_2_23_5_1","doi-asserted-by":"publisher","DOI":"10.1097\/MPA.0000000000000368"},{"key":"e_1_2_23_6_1","doi-asserted-by":"publisher","DOI":"10.3390\/NU13010159"},{"key":"e_1_2_23_7_1","doi-asserted-by":"crossref","unstructured":"K.Stopa A.Kusiak andM.Szopa P.F.\u2010I.J. of Undefined 2020. 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