Our previous study suggested that myeloid leukemia cells have abnormal energy metabolism [11], and that TIGAR (TP53 inducing glycolysis and apoptosis regulator) is highly expressed in myeloid leukemia cell lines and AML primary cells and associated with poor prognosis in adult patients with cytogenetically normal AML, which can be inhibited by DAC [12]. This evidence concerns the gene TIGAR and myeloid leukemia.