Recent studies demonstrated that somatic mutations within the ATP-binding pocket of the tyrosine kinase domain of the EGFR, including small in-frame deletions and missense substitutions, are present in a subset of lung adenocarcinomas and confer susceptibility to the gefitinib in lung cancer patients (Lynch et al, 2004; Paez et al, 2004). This evidence concerns the gene EGFR and lung carcinoma.