This was indeed shown in an in vitro study in which the cMET small inhibitor E7050 has the ability to circumvent resistance to the reversible, irreversible, and mutant-selective EGFR-TKIs induced by exogenous and/or endogenous HGF in EGFR mutant lung cancer cell lines, by blocking the Met/Gab1/PI3 K/Akt pathway in vitro [24]. This evidence concerns the gene EGFR and lung carcinoma.