Therefore, during disease transformation from MDS to AML, we observed a significant alteration in clonal architecture characterized by the replacement of the dominant TET2 single-mutated clone (C1) with triple-mutated clones that evolved via the emergence of the FLT3-TKD mutation in the pre-existent double-mutated clones TET2N191Kfs*4/RUNX1R201Q_HET and TET2N191Kfs*4/RUNX1R201Q_HOM (C2–C3). The gene discussed is FLT3; the disease is myelodysplastic syndrome.