Molecular lesions in AML cells occur mainly at two distinct levels: The activation of cytoplasmic tyrosine kinases (FLT3; KIT) or signaling modulators such as NRAS and secondary lesions that alter the function of certain transcription factors or epigenetic regulators, such as CEBPα, RUNX1, RUNX1T, RAR and KMT2A [1,4]. This evidence concerns the gene RUNX1 and acute myeloid leukemia.