MET can be activated as a primary oncogenic driver in NSCLC in at least two main ways: high-levelMET amplification andMET exon 14 alterations.MET exon 14 skipping events occur in both adenocarcinoma and squamous cell carcinoma histology and are found across all smoking histories and histologic types.MET exon 14 skipping results from somatic mutations in the introns ofMET and leads to an alternatively spliced transcript of MET49,50. Here, MET is linked to adenocarcinoma.