Sporadic literatures support the possibility of a linkage between mTOR activity and tumor-initiating cell maintenance or expansion [40–42], and the blockage of Akt/mTOR signaling could diminish cyclin G1-mediated sex determining region Y box 2 (SOX2) induction, and suppress self-renewal, chemoresistance, and tumorigenicity of hepatoma cells [43]. This evidence concerns the gene MTOR and neoplasm.