Regarding the possible mechanism of different distributions of CD8+ T, Tfh, and Th17 cells in HNSCC patients with high or low expressed PRAS40, there are some clues from the molecular landscape alternations in PRAS40 knockout HNSCC cells: the overall effects of TGF-β, PI3K-Akt, NF-κB, and mTORC1 signaling. This evidence concerns the gene TGFB1 and head and neck squamous cell carcinoma.