MET has been shown to be a key downstream mediator of EGFR-induced invasiveness in EGFR-dependent NSCLC cells, suggesting that therapeutic inhibition of MET in combination with EGFR blockade may prevent tumor metastasis beyond the effect of EGFR alone in a subset of lung cancers, in addition to the potential benefit of preventing the emergence of resistance through MET amplification [57]. This evidence concerns the gene MET and neoplasm.