To date, overexpression of AXL has been implicated in resistance to imatinib (BCR-Abl, c-Kit and PDGFR inhibitor), lapatinib (HER2 inhibitor), erlotinib (EGFR inhibitor) and cetuximab (EGFR-targeting monoclonal antibody), as well as resistance to the chemotherapeutics doxorubicin, cisplatin and etoposide (VP-16) in a variety of solid tumor types and blood cancers [26, 27, 31, 38, 39, 41, 42]. Here, AXL is linked to hematopoietic and lymphoid system neoplasm.