Since the CTCF binding site upstream of the EVI1 promoter was preserved in AML harbouring 3q21 rearrangements and seemed to be essential to SE hijacking, it has been proposed that the mechanism providing SE-promoter interaction is common for all 3q26-rearranged AMLs demonstrating EVI1 overexpression. This evidence concerns the gene RUNX1 and acute myeloid leukemia.