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We systematically identified regulators of this cell state using genome-wide CRISPR screens in primary T cells\n                  <jats:italic>in vitro<\/jats:italic>\n                  . Using random barcodes to link clonal relationships with guide identity and transcriptional states in single cells, we inferred differentiation trajectories and differentiation rates of CD8 T cells in tumors, while mitigating confounding clonal bias. We found that Trim28-deficient T cells in tumors were enriched in the TCF7+ cell state, depleted in cycling and terminal effector states, and uniquely generated a tissue-resident memory (TRM)-like state with increased chromatin accessibility at known TRM loci as well as repeat elements. Despite the increase in TCF7+ CD8 T cells, loss of Trim28 did not improve tumor control, likely because of reduced effector differentiation, highlighting the need for tuning the balance and dynamics of stem-like versus effector states for effective tumor clearance.\n                <\/jats:p>","DOI":"10.64898\/2026.06.14.732162","type":"posted-content","created":{"date-parts":[[2026,6,17]],"date-time":"2026-06-17T14:30:16Z","timestamp":1781706616000},"source":"Crossref","is-referenced-by-count":0,"title":["Discovery of Tcf7 regulators with clonally-resolved CRISPR screens identifies Trim28 as a mediator of CD8 T cell differentiation in tumors"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3869-0150","authenticated-orcid":false,"given":"Marc A.","family":"Schwartz","sequence":"first","affiliation":[{"name":"Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA, USA"},{"name":"Division of Hematology\/Oncology, Boston Children\u2019s 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