Several groups have identified somatic mutations in EGFR in patients with lung carcinoma with increased frequency in patients who are nonsmokers, female patients, and patients from East Asian parts.17 Nearly 90% of these mutations are present in first four exons (18‐21) of tyrosine kinase domain of the EGFR gene, which are either an in‐frame deletion in exon 19 or a missense mutation in exon 21.18, 19, 20, 21, 22 Other tyrosine kinases involved in resistance mechanism include insulin‐like growth factor 1 receptor, KRAS mutations, and the epithelial‐to‐mesenchymal transition.23 The gene discussed is EGFR; the disease is lung carcinoma.