MTOR and neoplasm: In HNSCC, EGFR is overexpressed in more than 90% of cases [80], where its activation triggers dysregulated oncogenic signaling via four major pathways: the Ras/Raf/MEK/ERK-MAPK cascade, which promotes cell proliferation and survival; the PI3K/AKT/mTOR pathway, which enhances cell survival, growth, and metabolism; the PLCγ/PKC axis, which contributes to tumor growth and metastasis; and the JAK/STAT signaling pathway, which mediates immune evasion and promotes chronic inflammation [91].