In addition, because DOT1L inhibition influenced CD14 and CD11b expression in all AML cell lines, it can be assumed that DOT1L-mediated H3K79me2 regulates the expression of several genes involved in myeloid differentiation, and, consequently, the loss of this epigenetic marker induces terminal myeloid differentiation in AML cells, irrespectively of MLL-r. The gene discussed is KMT2A; the disease is acute myeloid leukemia.