Summarizing, in the context of hematological tumors, AML LICs (with IDH1/2wt, TET2wt, EZH2wt genotype) present high levels of BCAT1, which catalyzes BCAA degradation and the depletion of α-KG, which reduces the activity of demethylases such as TET2 and prolyl hydroxylases such as EGLN1 (leading to DNA hypermethylation and stabilization of HIF-1α). This evidence concerns the gene TET2 and acute myeloid leukemia.