Epidermal growth factor receptor (EGFR) is overexpressed in > 90% of patients with HNSCC, and activation of EGFR has been linked to several immunosuppressive features within the tumor microenvironment, including limited infiltration by cytotoxic T cells, suppression of antigen presentation pathways, and an increase in regulatory T‐cell (Treg) recruitment [11, 12, 13]. The gene discussed is EGFR; the disease is neoplasm.