The epidermal growth factor receptor (EGFR) and its ligands promote the malignant behaviour of different tumours by cellular processes such as proliferation, differentiation, antiapoptotic signalling, angiogenesis, and metastasis.1 EGFR is overexpressed in up to 90% of head and neck squamous cell carcinomas (HNSCC), associated with an unfavourable prognosis.2 By EGFR phosphorylation intracellular signalling cascades, for example, Ras/Raf/MAPK (mitogen-initiated protein kinase) and PI3K/AKT (phosphatidylinositol 3-kinase) are activated, which mediate cellular proliferation and survival.3,4. This evidence concerns the gene EGFR and neoplasm.