Carcinogen-related HNSCC enhances VEGF production and consequently M2-cell migration and stabilization within the tumor, with TGF-β secretion [45], which promotes the epithelial–mesenchymal transition (EMT), angiogenesis, and cancer-associated fibroblast (CAF) activation, which in turn produces more TGF-β and angiogenic factors, leading to an immunosuppressive loop mechanism [108,109]. This evidence concerns the gene TGFB1 and head and neck squamous cell carcinoma.