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Hyperactivation of the Nrf2 pathway by genetic ablation of\n                    <jats:italic toggle=\"yes\">Keap1<\/jats:italic>\n                    or endogenous engineering of clinically observed\n                    <jats:italic toggle=\"yes\">Keap1<\/jats:italic>\n                    or\n                    <jats:italic toggle=\"yes\">Nfe2l2<\/jats:italic>\n                    mutations enhances tumor susceptibility to CAR T cell therapy. Thus, tumor-intrinsic molecular stress phenotypes can induce unexpected cell state\u2013specific vulnerabilities to cell-based immunotherapies. These findings provide a foundation to improve efficacy of CAR T cell therapy in solid malignancies and to better stratify patients with cancer by tumor genotype.\n                  <\/jats:p>","DOI":"10.1126\/sciadv.aeh8973","type":"journal-article","created":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T17:59:16Z","timestamp":1790963956000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":0,"title":["Tumor cell\u2013intrinsic stress states drive sensitivity to CAR T cell therapy in pancreatic cancer"],"prefix":"10.1126","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8179-1777","authenticated-orcid":true,"given":"Julia","family":"Fr\u00f6se","sequence":"first","affiliation":[{"name":"The David H. 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