Interestingly, some of the transcription factors known to bind to the GATA2 enhancer at 3q21, for example, ERG, GATA2, LMO2, and RUNX1, are reported to also interact with the loci involved in these atypical 3q26 translocations.87 All in all, it is possible that atypical 3q26 rearrangements and the classical inv(3)/t(3;3)(q21;q26) constitute a single AML entity that is characterized by elevated EVI1 levels through enhancer hijacking, absent MDS-EVI1 and a reduction in GATA2, while clinically sharing a poor prognosis and the occurrence of resistance to chemotherapy. This evidence concerns the gene GATA2 and myelodysplastic syndrome.