Several studies showed that gain-of-function somatic mutations affecting the catalytic domain (specifically the ATP binding site, exons 18–21) of EGFR in non-small cell lung carcinomas were strongly associated with response to gefitinib and erlotinib, both related EGFR-tyrosine kinase inhibitors (TKI) [3-5]. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.