AKT1 and glioblastoma: Further, the overexpression and silencing approach displayed that mTORC1 activation or silencing of mTORC2 inhibited the CSC population and tumorigenicity by suppressing the expression of EpCAM in HCC.132 The activation of the PI3K/AKT pathway was noticed in glioblastoma multiforme (GBM) neurospheres.