TET2 and acute myeloid leukemia: In vitro and in vivo analysis of separate exposure of Flt3ITD;Tet2-mutant AML monomorphic CD48+CD150− multipotent progenitor cells to 5-Aza and the mIDH2 inhibitor enasidenib led to partial normalization of cell differentiation, as well as reversal in many sites of known DNA hypermethylation induced by Tet2. However, in vivo RNA sequencing indicated that neither agent alone significantly suppressed the malignant progenitor clone.