This included tumor models without basal overexpression of EGFR and thus without primary susceptibility towards EGFR inhibition, as well as cell lines with genomic HER2 or MET amplification, for testing whether constitutive activation of other, RTK-dependent signalling pathways may represent a principle obstacle to the induction of acquired vulnerability to EGFR inhibitors. The gene discussed is EGFR; the disease is neoplasm.