Among kinase candidates to be targeted in epithelial cancers, the epidermal growth factor receptor (EGFR) was one of the first choices [10] based on the evidence in human tumor samples for oncogenic EGFR activation through EGFR gene amplification, gain-of-function deletions in the EGFR extracellular domain, and coexpression of EGFR and its ligands [11]. The gene discussed is EGFR; the disease is neoplasm.