The underlying mechanism of forced EVI1 or MEL1 transcription and co-silencing of GATA2 in 3q-rearranged AML is the repositioning of a GATA2 distal hematopoietic enhancer (G2DHE) into the vicinity of these EVI1 homologs [16, 18, 20]. This evidence concerns the gene RUNX1 and acute myeloid leukemia.