In NSCLC cells uncontrolled activation of the signaling induced by the hepatocyte growth factor (HGF) and its receptor, the Mesenchymal-Epithelial Transition factor (MET), can be triggered by increased HGF levels, receptor overexpression due to MET-amplification or post-transcriptional modifications, point-mutations of MET TK-domain and other functional domains, or reduced MET-degradation due to MET exon 14 splicing-site mutants resulting in exon 14 skipping/deletion. This evidence concerns the gene TKT and non-small cell lung carcinoma.