In this study, we report that in HNSCC, CXCL8 expression is activated via NF-κB/p65 protein phosphorylation at the Ser536 site by ROS induced under conditions of glucose deficiency, whereas CXCL8 increases CLU expression in TAMs to facilitate antioxidative stress in cancer cells. This evidence concerns the gene NFKB1 and head and neck squamous cell carcinoma.