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In this study, natural killer (NK) cells from patients with glioma show impaired oxidative phosphorylation and mitochondrial complex I activity. Multiomics profiling identified complex I subunit NDUFA9 as a critical mediator of NK cell metabolic fitness. The abundance of NDUFA9+ NK cells informed patient outcomes. Ndufa9 knockout in NK cells compromised mitochondrial function, antitumor efficacy, and the memory-like phenotype of NK cells by triggering a metabolic reprogramming toward glutamine dependence. The decreased \u03b1-ketoglutarate\/succinate ratio in Ndufa9-deficient NK cells mediated widespread epigenetic reprogramming by inducing the transcriptionally repressive histone mark H3K27me3 on key immune function genes. Resveratrol-mediated NDUFA9 activation or its overexpression enhanced NK cell anti-GBM function by restoring complex I activity. Together, these findings reveal the critical role of mitochondrial complex I activity in NK cells and highlight its potential as an actionable target to enhance NK cell\u2013based immunotherapy for patients with GBM.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Significance:<\/jats:title>\n                    <jats:p>This study reveals that NDUFA9 deficiency in mitochondrial complex I compromises metabolic fitness and impairs the antitumor activity of NK cells in GBM. We identify the mitochondrial complex I subunit NDUFA9 as a key pharmacologically targetable node for NK cell\u2013based immunotherapy in GBM, leveraging metabolic reprogramming to enhance antitumor efficacy.<\/jats:p>\n                    <jats:p>See related commentary by Tiberti et al., p. 1727<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1158\/2159-8290.cd-25-0643","type":"journal-article","created":{"date-parts":[[2026,4,7]],"date-time":"2026-04-07T12:45:54Z","timestamp":1775565954000},"page":"1924-1949","update-policy":"https:\/\/doi.org\/10.1158\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Correcting Mitochondrial Complex I Defect in Tumor-Associated Natural Killer Cells Potentiates Immunotherapy for Glioblastoma"],"prefix":"10.1158","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0009-0008-9565-0757","authenticated-orcid":false,"given":"Nianxin","family":"Zhou","sequence":"first","affiliation":[{"name":"1Department of Neurosurgery, West China Hospital, State Key Laboratory of Biotherapy, Sichuan University and Collaborative Innovation Center, Chengdu, P. 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