EGFR and neoplasm: Common mechanisms of resistance to ATP-competitive EGFR tyrosine kinase inhibitors such as gefitinib and erlotinib are the T790M “gatekeeper” mutation in the EGFR kinase domain [12], and amplification and/or overexpression of the MET and AXL receptor tyrosine kinases [13, 14], which take over the function of inhibited EGFR to sustain tumor growth.