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Leukemia subtypes with hallmark overexpression of <jats:italic>HOXA9<\/jats:italic> include those carrying <jats:italic>MLL<\/jats:italic> gene rearrangements, <jats:italic>NPM1c<\/jats:italic> mutations, and other genetic alternations. A growing body of evidence indicates that <jats:italic>HOXA9<\/jats:italic> dysregulation is both sufficient and necessary for leukemic transformation. The HOXA9 mRNA and protein regulation includes multilayered controls by transcription factors (such as CDX2\/4 and USF2\/1), epigenetic factors (such as MLL\u2010menin\u2010LEDGF, DOT1L, ENL, HBO1, NPM1c\u2010XPO1, and polycomb proteins), microRNAs (such as miR\u2010126 and miR\u2010196b), long noncoding RNAs (such as HOTTIP), three\u2010dimensional chromatin interactions, and post\u2010translational protein modifications. Recently, insights into the dynamic regulation of HOXA9 have led to an advanced understanding of the HOXA9 regulome and provided new cancer therapeutic opportunities, including developing inhibitors targeting DOT1L, menin, and ENL proteins. This review summarizes recent advances in understanding the molecular mechanisms controlling HOXA9 regulation and the pharmacological approaches that target HOXA9 regulators to treat HOXA9\u2010driven acute myeloid leukemia.<\/jats:p>","DOI":"10.1111\/febs.16268","type":"journal-article","created":{"date-parts":[[2021,11,7]],"date-time":"2021-11-07T13:10:33Z","timestamp":1636290633000},"page":"321-339","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":45,"title":["Molecular regulators of HOXA9 in acute myeloid leukemia"],"prefix":"10.1111","volume":"290","author":[{"given":"Sajesan","family":"Aryal","sequence":"first","affiliation":[{"name":"Division of Hematology and Oncology &amp; O\u2019Neal Comprehensive Cancer Center University of Alabama at Birmingham  AL USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yang","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Tumor Cell 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