mutations; class 2 mutations; CEBPA, NPM1 (transcription factors), and MLL, prevent apoptosis of the cell and disrupt its differentiation.4 In addition, epigenetic mutations such as TET, ASXL1, IDH1, IDH2, EZH2, DNMT3, and RNA splicesome mutations such as U2AF1, SRSF2, ZRSR2, SF3B1, and tumor suppressors such as WT1 and TP53 have been blamed in the pathogenesis of AML.5 Age, performance status of the patient, comorbid diseases, MDS, and myeloproliferative disease history as well as genetic characteristics are determinant in the prognosis of AML. This evidence concerns the gene ASXL1 and acute myeloid leukemia.