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Forced expression of C\/EBP\u03b1 in B cells was reported to cause loss of B\u2010cell identity due to the inhibition of Pax5, a master regulator of B\u2010cell differentiation; however, it is not known whether the same mechanism is applicable for B\u2010ALL development by <jats:italic>CEBPA\u2010IGH<\/jats:italic>. It is known that a full\u2010length isoform of C\/EBP\u03b1, p42, promotes myeloid differentiation, whereas its N\u2010terminal truncated isoform, p30, inhibits myeloid differentiation through the inhibition of p42; however, the differential role between p42 and p30 in ALL development has not been clarified. In the present study, we examined the effect of the expression of p42 and p30 in B cells by performing RNA\u2010seq of mRNA from LCL stably transfected with p42 or p30. Unexpectedly, suppression of PAX5 target genes was barely observed. Instead, both isoforms suppressed the target genes of MEF2 family members (MEF2s), other regulators of B\u2010cell differentiation. Similarly, MEF2s target genes rather than PAX5 target genes were suppressed in <jats:italic>CEBP\u2010IGH<\/jats:italic>\u2010positive ALL (<jats:italic>n<\/jats:italic>\u00a0=\u00a08) compared with other B\u2010ALL (<jats:italic>n<\/jats:italic>\u00a0=\u00a0315). Furthermore, binding of both isoforms to MEF2s target genes and the reduction of surrounding histone acetylation were observed in ChIP\u2010qPCR. Our data suggest that the inhibition of MEF2s by C\/EBP\u03b1 plays a role in the development of <jats:italic>CEBPA\u2010IGH<\/jats:italic>\u2010positive ALL and that both isoforms work co\u2010operatively to achieve it.<\/jats:p>","DOI":"10.1111\/cas.15641","type":"journal-article","created":{"date-parts":[[2022,11,7]],"date-time":"2022-11-07T09:19:45Z","timestamp":1667812785000},"page":"781-792","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Functional inhibition of MEF2 by C\/EBP is a possible mechanism of leukemia development by <i>CEBP\u2010IGH<\/i> fusion gene"],"prefix":"10.1111","volume":"114","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8523-7119","authenticated-orcid":false,"given":"Koya","family":"Odaira","sequence":"first","affiliation":[{"name":"Department of Integrated Health Sciences, Division of Cellular and Genetic Sciences Nagoya University Graduate School of Medicine  Nagoya 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