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Here, we interrogated gene expression and whole-genome CRISPR\/Cas9 screening in a large panel of patient-derived GSCs, differentiated GBM cells (DGC), and neural stem cells (NSC) to identify master regulators of GSC stemness, revealing an essential transcription state with increased RNA polymerase II\u2013mediated transcription. The YY1 and transcriptional CDK9 complex was essential for GSC survival and maintenance in vitro and in vivo. YY1 interacted with CDK9 to regulate transcription elongation in GSCs. Genetic or pharmacologic targeting of the YY1\u2013CDK9 complex elicited RNA m6A modification\u2013dependent interferon responses, reduced regulatory T-cell infiltration, and augmented efficacy of immune checkpoint therapy in GBM. Collectively, these results suggest that YY1\u2013CDK9 transcription elongation complex defines a targetable cell state with active transcription, suppressed interferon responses, and immunotherapy resistance in GBM.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Significance:<\/jats:title>\n                    <jats:p>Effective strategies to rewire immunosuppressive microenvironment and enhance immunotherapy response are still lacking in GBM. YY1-driven transcriptional elongation machinery represents a druggable target to activate interferon response and enhance anti\u2013PD-1 response through regulating the m6A modification program, linking epigenetic regulation to immunomodulatory function in GBM.<\/jats:p>\n                    <jats:p>This article is highlighted in the In This Issue feature, p. 275<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1158\/2159-8290.cd-20-1848","type":"journal-article","created":{"date-parts":[[2022,1,13]],"date-time":"2022-01-13T10:45:15Z","timestamp":1642070715000},"page":"502-521","update-policy":"https:\/\/doi.org\/10.1158\/crossmark_policy","source":"Crossref","is-referenced-by-count":82,"title":["Transcription Elongation Machinery Is a Druggable Dependency and Potentiates Immunotherapy in Glioblastoma Stem 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Z.","family":"Shen","sequence":"additional","affiliation":[{"name":"3Tumor Initiation and Maintenance Program, NCI-Designated Cancer Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, California."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhengyu","family":"Liang","sequence":"additional","affiliation":[{"name":"4Department of Cellular and Molecular Medicine, Institute of Genomic Medicine, University of California, San Diego, La Jolla, California."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiulian","family":"Wu","sequence":"additional","affiliation":[{"name":"1Hillman Cancer Center and Department of Neurology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania."},{"name":"2Division of Regenerative Medicine, Department of Medicine, University of California, San Diego, La Jolla, 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