Nonetheless, it is usually accompanied by concomitant mutations, including but not limited to FLT3-ITD (FMS-like receptor tyrosine kinase-3 internal tandem duplication), DNMT3A (DNA methyltransferase 3 alpha), IDH1/2 (isocitrate dehydrogenase 1⁄2), and TET2 (Tet Methylcytosine Dioxygenase), raising speculation of synergistic interactions that promote AML transformation and progression [3,47,48,49]. This evidence concerns the gene FLT3 and acute myeloid leukemia.