FLT3-ITD mutations concentrated in the juxtamembrane domain induce ligand-independent dimerization to activate phosphatidylinositol 3-kinase (PI3K)/AKT, mitogen-activated extracellular signal regulated kinase (MEK)/ERK and Janus Kinase (JAK)/STAT signal transduction pathways and achieve cytokine-independent cell proliferation and finally result in leukemia under the synergistic effect of other oncogenes [32]. Here, FLT3 is linked to leukemia.