Our findings provide evidence that the levels of the cancer cell-derived CXCL8 and its encoded protein IL-8 are increased under conditions of glucose deficiency to educate TAMs, facilitate antioxidative mechanisms, induce resistance to nutrient-starvation therapies, and serve as a therapeutic target for overcoming anlotinib resistance in HNSCC patients. The gene discussed is CXCL8; the disease is cancer.