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We therefore set out to study the role of RFX7 in B\u2009cell activation and lymphomagenesis. Here we show that\n                    <jats:italic>RFX7<\/jats:italic>\n                    truncations cause loss-of-function and dominant-negative effects. Moreover, low\n                    <jats:italic>RFX7<\/jats:italic>\n                    mRNA levels correlate with worse diffuse large B\u2009cell lymphoma prognosis. Accordingly,\n                    <jats:italic>Rfx7<\/jats:italic>\n                    deletion in B\u2009cells accelerates pathogenesis in mouse Bcl6- and p53-loss-driven B\u2009cell lymphoma models. Rfx7-deficient B\u2009cells exhibit increased Myc activity and enhanced germinal center B\u2009cell and plasmablast responses. These alterations are reverted by Myc haploinsufficiency, which provides partial protection from nonsymptomatic\n                    <jats:italic>p53<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <jats:italic>Rfx7<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    B\u2009cell lymphoma, but does not prevent detrimental Myc deregulation in aggressive disease. Deletion of\n                    <jats:italic>Aicda<\/jats:italic>\n                    , which favors genomic alterations in activated B\u2009cells, limits lymphoma development in the\n                    <jats:italic>p53<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <jats:italic>Rfx7<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    double-hit mouse model. These results indicate that Rfx7 represses B\u2009cell activation, Myc activity, and Myc- and activation-induced cytidine deaminase (AID)-dependent pro-lymphomagenic processes.\n                  <\/jats:p>","DOI":"10.1038\/s41590-026-02526-2","type":"journal-article","created":{"date-parts":[[2026,6,1]],"date-time":"2026-06-01T09:02:08Z","timestamp":1780304528000},"page":"1490-1501","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Regulatory factor X 7 limits Myc activity during B cell activation and suppresses Myc-dependent lymphomagenesis"],"prefix":"10.1038","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0009-0008-2788-5407","authenticated-orcid":false,"given":"Berenice A.","family":"Fischer","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1737-0388","authenticated-orcid":false,"given":"Hanif J.","family":"Khameneh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5421-8003","authenticated-orcid":false,"given":"Jessica","family":"Guerra","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2837-7638","authenticated-orcid":false,"given":"Alessandro","family":"Zenobi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jasmine","family":"Ciorciari","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Irene","family":"Buzzago","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria Serena","family":"Merli","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohammed","family":"Said","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pedro M. 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The corrected source data is now available online.","order":7,"name":"change_details","label":"Change Details","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"9 October 2026","order":8,"name":"change_date","label":"Change Date","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"Update","order":9,"name":"change_type","label":"Change Type","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"This article was originally published under the subscription model but it is now published under an Open Access license.","order":10,"name":"change_details","label":"Change Details","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"M.A.S. receives research funding from Genentech, Novartis, Merck, Bristol Myers Squibb, AstraZeneca and Abbvie (Institution) and is on the advisory board of AstraZeneca. D.W.S. has received honoraria from Abbvie, AstraZeneca, Chugai, Kite\/Gilead and Roche and research funding from Roche\/Genentech. Unrelated to this work, F.B. has received institutional research funds from ADC Therapeutics, Bayer AG, BeiGene, Floratek Pharma, Helsinn, HTG Molecular Diagnostics, Ideogen AG, Idorsia Pharmaceuticals Ltd., Immagene, ImmunoGen, Menarini Ricerche, Nordic Nanovector ASA, Oncternal Therapeutics and Spexis AG; consultancy fee from BIMINI Biotech, Floratek Pharma, Helsinn, Immagene, Menarini and Vrise Therapeutics; advisory board fees to institution from Novartis; and travel grants from Amgen, Astra Zeneca and iOnctura. D.R. has received honoraria from AstraZeneca, BeOne, Lilly and Takeda, research grants from AbbVie, AstraZeneca and Janssen, and travel grants from AstraZeneca, Janssen and Roche. Unrelated projects in G.G.\u2019s laboratory are supported by OM Pharma. The other authors declare no competing interests.","order":1,"name":"Ethics","label":"Competing interests","group":{"name":"EthicsHeading","label":"Ethics"}}]}}