A major driver is receptor tyrosine kinase (RTK) signaling, particularly via the epidermal growth factor receptor (EGFR), which is overexpressed in 80–90% of HNSCC cases and signals downstream through PI3K, AKT, and mTOR to fuel tumor growth [55,56,57,58]. The gene discussed is MTOR; the disease is head and neck squamous cell carcinoma.