 EGFR tyrosine kinase mutation is frequently seen in our NSCLC, especially adenocarcinoma.1 The epidermal growth factor receptor EGFR of receptor tyrosine kinases TKs regulate many developmental, metabolic and physiological processes. In tumor cells, the TK activity of EGFR may be dysregulated by several mechanisms, including EGFR gene mutation, increased gene copy number and EGFR protein overexpression.1 Improper activation of EGFR TK results in increased malignant cell survival, proliferation, invasion and metastasis. EGFR overexpression is observed in tumors from more than 60 of patients with metastatic non-small-cell lung cancer NSCLC and is correlated with poor prognosis.2 Treatment with the reversible EGFR TK inhibitors TKIs, gefitinib and erlotinib, results in dramatic antitumor activity in a subset of patients with NSCLC. Sequencing of the EGFR gene revealed that a majority of tumors responding to EGFR TKIs harbored mutations in the TK domain of EGFR. For patients whose tumors exhibit EGFR mutations, the response rate to gefitinib and erlotinib is approximately 75, suggesting that these mutations, at least in part, drive malignant transformation. 