One way that this could be achieved by pharmacologic BET bromodomain inhibition.110,111 Indeed, in both 3q-rearranged cell lines as well as primary t(3;3) AML patient samples, treatment with the BET bromodomain inhibitor JQ1 led to a decrease of EVI1 and growth arrest of the AML cells.77 Other studies have specifically investigated the binding of important myeloid transcription factors to the GATA2 distal hematopoietic enhancer that is often relocated to the EVI1 locus, including CEBPA and RUNX1. The gene discussed is CEBPA; the disease is acute myeloid leukemia.