For example, in the treatment of non-small cell lung cancer (NSCLC) and colorectal cancers with anti-EGFR agents (erlotinib, gefitinib), resistant tumors exhibit a significantly higher proportion of MET receptor amplifications, another receptor tyrosine kinase (RTK) for the hepatocyte growth factor (HGF), that is frequently present in those tumor microenvironments [11–13]. This evidence concerns the gene MET and non-small cell lung carcinoma.