AKT1 and glioblastoma: Although no direct evidence is available regarding the involvement of CTSS and CTSL in the PI3K/Akt/mTOR pathway in HCC proliferation, the observation that in glioblastoma cells, the inhibition of CTSS reduces the phosphorylation of Akt [77] suggests that the involvement of cathepsins in this pathway is common in different types of cancers, including HCC.