KDM5A translocation with NUP98 was frequently found to be pathogenic in AML patients, and KMD5A downregulation suppressed proliferation and induced the apoptosis of AML cells.428,429 The loss or inhibition of KDM5D promoted cell differentiation, impeded the growth of APL cells, and improved sensitivity to all-trans retinoic acid treatment.430KDM5B was overexpressed in CML, and mediated myeloid differentiation and Toll-like receptors via GATA and AP-1 transcription factors. This evidence concerns the gene KDM5D and acute myeloid leukemia.