AKT1 and neoplasm: Most importantly, in an inducible tissue-specific spontaneous HNSCC mouse model with 100% penetrance by the combined deletion of Tgfbr1 and Pten (Tgfbr1/Pten 2cKO) in the oral mucosa21 with ubiquitous activation of the Akt/mTOR/survivin pathway,22 YM155 exerted significant therapeutic effects by delaying tumor onset and suppressing tumor growth.