Mechanisms of EGFR resistance continue to be a topic of interest in different tumor types including SCCHN where several possible mechanisms have been described including a deletion mutation of exon 2–7 of the extracellular ligand-binding domain of EGFR leading to a truncated form of EGFR (EGFR vIII) that is auto-phosphorylated in a ligand-independent way. Here, EGFR is linked to neoplasm.