Faden DL, et al. - A total of 20 head and neck squamous cell carcinoma (HNSCC) tumors were prospectively examined to evaluate the mechanisms of immune escape from epidermal growth factor receptor-specific monoclonal antibody (mAb) therapy in HNSCC cases. Researchers evaluated the expression of killer-cell immunoglobulin-like receptor (KIR) and human leukocyte antigen-C (HLA-C) along with the impact of KIR blockade in HNSCC cell lines. They observed a higher rate of mutations in HLA-C vs responders and HNSCC tumors in The Cancer Genome Atlas, among participants who did not respond to cetuximab. Induction of upregulation of HLA-C on HNSCC cells via interferon gamma was noted due to cetuximab-activated natural killer (NK) cells (in vitro). They reported an increased killing of HNSCC cells while treating with the anti-KIR mAb lirilumab. They concluded a provision of mechanism of immune evasion through disruption of NK activation due to alterations in HLA-C.