In addition, they more often present disease-related characteristics associated with a poorer prognosis such as complex karyotype, ASXL1, RUNX1 or TP53 mutations and/or secondary AML evolving from myelodysplastic syndrome or myeloproliferative disorders or after previous exposure to cytotoxic treatments (therapy-related AML) [6, 7]. This evidence concerns the gene RUNX1 and acute myeloid leukemia.