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Morphologically, the leukemic cells are large and agranular blasts mimicking lymphoblasts and negative for cytochemical reactions of myeloperoxidase (MPO), Sudan Black B, or nonspecific esterase [1]. The immunophenotypic characteristics of AML-M0 blasts are low expression of MPO, positive for at least one myeloid antigen (CD13, CD33, CD15, or CD11b), frequent expression of stem cell�Cassociated antigens (CD34, HLA-DR, CD117), TdT, and occasional coexpression of lymphoid-associated antigens (CD7 or CD19) [1]?and?[3]. As for cytogenetic abnormalities, despite that the incidence of abnormal, complex, or unbalanced chromosomal changes has been reported to be more frequent, there are no recurrent or specific cytogenetic abnormalities in AML-M0 Tenofovir cell line [3]. In AML, gene mutations not only have an implication in molecular pathogenesis but also provide a prognostic relevance in addition to the cytogenetic subtypes [4]. Previous studies have focused on class I and class II mutations in AML-M0 [5], [6], [7]?and?[8]. The development of AML was oftentimes caused by at least two-hit process mostly by class I and class II mutations. The class I mutation is defined by activating mutations of receptor tyrosine kinases and RAS signaling pathways, and the class II mutation is loss-of-function mutations of hematopoietic transcription factors [9]. RUNX1 mutation was the Sitaxentan most common gene mutation described in AML-M0 [5]. FLT3 mutation was also reported as a recurrent gene mutation, whereas RAS and PTPN11 mutations were less frequent in AML-M0 [6], [7]?and?[8]. Other gene mutations with prognostic relevance have not been studied comprehensively in AML-M0, including mutated genes of epigenetic regulators, such as IDH1, IDH2, TET2, DNMT3A, ASXL1, and EZH2 genes [10], [11], [12]?and?[13]. We thus examined a wide spectrum of gene mutations, including class I genes of activated signaling pathways (FLT3-ITD, FLT3-TKD, C-FMS, KIT, N-RAS, K-RAS, PTPN11, and JAK2V617F), class II genes affecting hematopoietic transcription and differentiation (RUNX1, NPM1, and CEBP��), class III genes of epigenetic check details regulators (IDH1, IDH2, TET2, DNMT3A, MLL-PTD, ASXL1, and EZH2), and class IV genes of tumor suppressors (WT1 and TP53) from the bone marrow cells of patients with AML-M0 at the initial diagnosis. The status of gene mutations was also correlated with the clinicohematological features to determine their clinical relevance in patients with AML-M0. From 1991 to 2010, a total of 67 patients fulfilling the diagnostic criteria of de novo AML-M0 at Chang Gung Memorial Hospital and Mackay Memorial Hospital was enrolled. The diagnosis of AML-M0 was made according to the French-American-British criteria: >?30% blasts in bone marrow,