Multiple mechanisms of drug resistance exerted by Axl have been reported, including overexpression of Axl in EMT-transformed cancer cells, decreased expression of microRNAs (miRs) targeting Axl, and heterodimerization of Axl with RTKs such as epidermal growth factor (EGF)-R, Her3, MET, platelet-derived growth factor (PDGF)-R, or FGFR-3 (Figure 1E) [45,46,47,48]. The gene discussed is AXL; the disease is cancer.