CCL5 and neoplasm: Besides, substantial infiltration of pro-inflammatory immune cells, such as tumor-associated macrophages (TAM), natural killer (NK) cells, and CD8+ T cells, HNSCC TME is immunosuppressive.34 Expression of pro-inflammatory mediators, such as IL-1α, IL-1β, IL-6, IL-8, TNF-α, TGF-β, granulocyte–macrophage colony-stimulating factor (GM-CSF), vascular endothelial growth factor (VEGF), monocyte chemoattractant protein 1 (MCP-1), RANTES (CCL5), and prostaglandin E2 (PGE2) are found to be upregulated in the premalignant lesions of HNSCC38,39 and are involved in progression and metastasis.