Survivin inhibition by YM155 downregulates the activation of the Akt/mTOR/S6 signaling pathway in a dose-dependent manner, which may delay tumor onset; this result is similar to the mTOR suppression in the transgenic mouse model of HNSCC in our previous report.25 These findings prove the essential role of survivin in carcinogenesis and further progression of HNSCC. The gene discussed is MTOR; the disease is neoplasm.