In acute myeloid leukemia (AML) with inv(3)/t(3;3), it was also found that targeting MYB or mutating its DNA-binding motif within the GATA2 enhancer resulted in myeloid differentiation and cell death, suggesting that interference with transcription of MYB downstream gene EVI1 provides a potential entry point for AML therapy [47]. This evidence concerns the gene MYB and acute myeloid leukemia.