EGFR drives tumorigenesis as a result of activating mutations in adenocarcinoma of the lung and by less defined mechanisms of pathway activation (increased expression of receptors or ligands) in other malignancies such as head and neck cancer, colorectal cancer, squamous cell carcinoma of the lung, and pancreatic cancer [1].Best responses and clinical benefit have been seen in malignancies with EGFR activating mutations but clinical benefit has also been observed in conditions where the pathway is not activated as a result of EGFR mutations. This evidence concerns the gene EGFR and lung adenocarcinoma.