The poor clinical response of NSCLC to anti-EGFR therapies is due to the primary and secondary resistance of cancer cells to these drugs, which is thought to occur via several mechanisms, including HER-2 amplification, MET amplification, mutation in exon 20 of EGFR (T790M), PI3K mutations, and transformation into small cell lung cancer (Antonicelli et al., 2013; Barr Kumarakulasinghe et al., 2015). This evidence concerns the gene EGFR and non-small cell lung carcinoma.