AKT1 and glioblastoma: Panner et al. [60,61] showed that TRAIL resistance in glioblastoma multiforme cells (GBM) is the result of c-FLIPS overexpression, and that activation of the Akt mammalian target of rapamycin (mTOR)-p70 S6 kinase 1 (S6K1) pathway leads to increased translation of the c-FLIPS protein.