In mice, it was shown that GATA2 haploinsufficiency cooperates with Evi1 overexpression and accelerates the onset of Evi1-induced leukemia,79 which appears to correlate with the observation that in humans, inherited GATA2 haploinsufficiency constitutes a predisposition to develop MDS or AML.80 Thus, this specific translocation can be considered to result in a “double hit” leading to malignant transformation. This evidence concerns the gene RUNX1 and myelodysplastic syndrome.