Mechanisms for oncogenic conversion of EGFR in cancer include EGFR gene amplification, structural rearrangements of the receptor, overexpression of epidermal growth factor (EGF)–family ligands by tumor cells and/or surrounding stroma, and—as was recently shown in lung cancer—activating mutations in the EGFR kinase domain [1]. The gene discussed is EGF; the disease is neoplasm.