FLT3 and cancer: Sorafenib-acquired resistance reportedly involves a variety of mechanisms, including multiple-signal pathway crosstalk; abnormal expression of tyrosine kinase receptors, such as PDGFR- β, c-kit, Flt-3, VEGFR and EGFR; epithelial-mesenchymal transition (EMT); and cancer stem-cell differentiation [16–18].