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Interferon regulatory factor 8 (IRF8) is a crucial transcription factor for hematological lineage commitment, but its role in T\u2010ALL is unclear. Here, IRF8 is shown to suppress T\u2010ALL. The expression of IRF8 is abnormally silenced in patients with T\u2010ALL. Knockout of\n                    <jats:italic>Irf8<\/jats:italic>\n                    significantly hastens the progression of Notch1\u2010induced T\u2010ALL in vivo. Overexpression of IRF8 suppresses the proliferation and invasion of T\u2010ALL cells by inhibiting the phosphatidylinositol 3\u2010kinase\/AKT signaling pathway. The fat mass\u2010 and obesity\u2010associated protein (FTO), an m6A demethylase, is responsible for directly binding to m6A sites in 3\u2032 untranslated region of\n                    <jats:italic>IRF8<\/jats:italic>\n                    messenger RNA (mRNA) and inducing mRNA degradation via m6A modification. Targeting the FTO\u2010IRF8 axis is used as a proof of concept therapy; inhibition of FTO's demethylase activity drastically alleviates the proliferation of leukemic cells and prolongs the survival of T\u2010ALL mice by restoring IRF8 expression. This study elucidates the pathogenesis of T\u2010ALL from the perspective of epitranscriptomics and provides new insight into the genetic mechanisms and targeted therapy of T\u2010ALL.\n                  <\/jats:p>","DOI":"10.1002\/advs.202201724","type":"journal-article","created":{"date-parts":[[2022,12,7]],"date-time":"2022-12-07T14:45:11Z","timestamp":1670424311000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":20,"title":["Silencing of\n                    <i>IRF8<\/i>\n                    Mediated by m6A Modification Promotes the Progression of T\u2010Cell Acute Lymphoblastic Leukemia"],"prefix":"10.1002","volume":"10","author":[{"given":"Ying","family":"Zhou","sequence":"first","affiliation":[{"name":"Department of Hematology Qilu Hospital Cheeloo College of Medicine Shandong University  Jinan 250012 P. R. 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