The mutation status of epidermal growth factor receptor (EGFR) acts as a significant molecular feature of lung adenocarcinoma patients and sensitizing EGFR mutations including in-frame deletion of exon 19 and L858R substitute mutation of exon 21 play a critical role in predicting the sensitivity to EGFR tyrosine kinase inhibitor (EGFR-TKI) (3–5). The gene discussed is EGFR; the disease is lung adenocarcinoma.