Depletion of JMJD1C inhibited cell growth and leukaemogenesis of MLL-AF9 cells by triggering apoptosis.52 JMJD1C had also been recently implicated in AML1-ETO-53 and HOXA9-mediated leukaemias.54 JMJD1C was identified as a coactivator in AETFC, a complex formed by AML1-ETO, where JMJD1C maintained low level of H3K9me2, hence enhancing gene expression of AML1-ETO targets. This evidence concerns the gene RUNX1 and leukemia.