These studies showed that the catalytic activity of CDK6 is required for this function because expression of a mutant form of CDK6 with disrupted kinase function is unable to block the differentiation induced by shRNA-mediated depletion of CDK6 in MLL-rearranged AML cells (Placke et al., 2014). The gene discussed is KMT2A; the disease is acute myeloid leukemia.