The tumor microenvironment (TME) of HNSCC is highly heterogeneous and predominantly immunosuppressive, characterized by macrophages and myeloid-derived suppressor cell recruitment (Canning et al., 2019), T cell and natural killer (NK) cell dysfunction, regulatory T cell (Treg) activation (Reichert et al., 2002), and alteration in cytokine release such as enhanced interleukin-10 (IL-10) and IL-6 production and reduced transforming growth factor β (TGF-β) and IL-12 secretion (Lathers and Young, 2004; Varilla et al., 2013). The gene discussed is IL6; the disease is neoplasm.