In patients with non-small-cell lung cancer (NSCLC), the possibility of treatment with tyrosine kinase inhibitor (TKI) is determined by the presence of mutations on exons 18–21 of the epidermal growth factor receptor (EGFR).1 Clinical evidence heightens the fact that EGFR-targeted therapy can significantly improve progression-free survival (PFS) and overall survival (OS) in patients.2,3 Therefore, assessing the status of EGFR mutations is important for potential EGFR-TKI therapy. This evidence concerns the gene EGFR and non-small cell lung carcinoma.