The combined treatment of DPI with FLT3-ITD inhibitors, such as midostaurin or sorafenib, has also been proposed to synergistically inhibit the proliferation of AML cell lines harboring FLT3-ITD, and its combination with the tyrosine kinase inhibitor imatinib has been shown to synergistically increase apoptosis in chronic myeloid leukemia (CML) cells in vivo [20]. The gene discussed is FLT3; the disease is acute myeloid leukemia.