A distinct molecular subset of non-small-cell lung cancer (NSCLC), driven by mutated EGFR, has been defined clearly and has become the subject of intense investigation in laboratories and clinics. Specific activating mutations in the tyrosine kinase domain of EGFR have been correlated with striking responses to EGFR tyrosine-kinase inhibitors (TKIs) such as erlotinib and gefitinib. EGFR TKIs alone or in combination with chemotherapy do not improve outcomes significantly compared with chemotherapy...