DOI: 10.1093/jnci/djp439

The epidermal growth factor receptor (EGFR) is a transmembrane glycoprotein that regulates various cellular processes, including cell proliferation, differentiation, and survival ( 1). Its dysregulation in various malignancies, including lung, gastrointestinal, and head and neck cancers, has been associated with poor prognosis and increased resistance to chemotherapy and radiotherapy ( 2). Monoclonal anti-bodies that act as EGFR inhibitors (EGFRIs), such as cetuximab and panitumumab, and small-molecule EGFRIs, such as erlotinib, gefi-tinib, and lapatinib, provide a rational approach to cancer therapy because they specifically inhibit EGFR signaling by preventing ligand binding in the extracellular domain or by blocking intracyto-plasmic phosphorylation, respectively ( 3). In addition to its prominent role in cancer, EGFR is constitutively expressed in epithelial tissues, such as skin and hair follicles, where it is critical for normal tissue function and reparative capability ( 1). As a consequence of this con