In acute myeloid leukemia (AML) the study of specific disease-defining translocations, such as t(15;17)-PML-RARα, t(8;21)-RUNX1-ETO or t(6;9)-DEK-CAN (also called DEK-NUP214) has allowed a better understanding of the molecular mechanisms of disease and recognition of the central role of aberrant transcription regulators in the pathogenesis of AML [1]. This evidence concerns the gene RUNX1 and acute myeloid leukemia.