EGFR and neoplasm: MET is a high affinity tyrosine kinase receptor for hepatocyte growth factor (HGF).[8] Derailment of normal MET signaling is associated with invasive growth, tumor progression and metastases; [9] aberrant MET signaling can result from MET over-expression, amplification or mutations, all of which are relevant in NSCLC.[4, 5, 6, 7] MET amplification predicts worse survival in NSCLC, [10] it has been implicated in 5–20% of patients with acquired resistance to EGFR TKI [11, 12, 13, 14] and correlates with response to MET inhibitor therapy [13].