The co-occurrence of IDH mutations in FLT3-ITD-subclones (e.g., IDH1) or in non-ITD AML cells (e.g., IDH2) upon giltertinib treatment provides a rationale for the use of IDH-inhibitors either as monotherapy (e.g., enasidenib) or combination therapy (e.g., ivosidenib). This evidence concerns the gene IDH2 and acute myeloid leukemia.