For example, during epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) treatment, secondary EGFR mutation T790M, MET proto-oncogene, receptor tyrosine kinase (MET, also known as hepatocyte growth factor receptor, HGFR) amplification, receptor tyrosine-protein kinase erbB-2 (ERBB2, also known as HER2) amplification as well as Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations are often detectable in relapsed lung cancer patients and known to contribute to drug resistance [13–15]. This evidence concerns the gene KRAS and lung carcinoma.