Chromatin immunoprecipitation (ChIP) experiments demonstrated an enhanced chromatin binding ability of MH to an array of target genes, including HDAC9. 1 The overexpression of HDAC9 has been shown to promote lymphoproliferative disorders and the development of lymphoma in Eμ-HDAC9 mouse models.14 Furthermore, our previous findings indicated that the higher affinity of MH fusion to the promoter of HDAC9 could be facilitated by HNRNPUL1 component in the protein complex.12 Overall, these observations underscore the critical role of HDAC9 dysregulated by MEF2D fusions in driving leukemogenesis. The gene discussed is HDAC9; the disease is lymphoproliferative syndrome.