In various tumour entities, aberrant activation of MET and AXL has been described in terms of resistance to RAS–RAF–MEK, mammalian target of rapamycin (mTOR), VEGFR therapies16, 38, 39 including sunitinib and sorafenib,16, 40 and, recently, immune evasion.41 The gene discussed is AXL; the disease is neoplasm.