A meta-analytical study showed that 66% of examined clinical HNSCC cases demonstrate an increase in pathway activity due to aberrant expression of key mediators of the PI3K-Akt-mTOR signaling pathway, including downregulation of the repressor PTEN and upregulation in the activity of PI3K catalytic subunits [14]. This evidence concerns the gene PTEN and head and neck squamous cell carcinoma.