It is worth noting that AML cells characterized by the t(8;21) translocation, represented here by KASUMI1 cells, also responded to MYB depletion with a myeloid commitment induction and a reduction of the proliferation capacity, though we failed to detect any MAFB expression, suggesting that in these cells MYB regulates a distinct programme of gene expression, further highlighting the complexity of aberrant transcriptional programmes brought about by different mutations. The gene discussed is MAFB; the disease is acute myeloid leukemia.