Malignant glioblastomas are known to be highly resistant to the proapoptotic effect of standard cancer therapy owing to constitutive activation of the phosphoinositide 3-kinase (PI3K)/Akt49, mammalian target of rapamycin (mTOR)50, or nuclear factor (NF)-κB51–53 signalling pathway54,55. Here, MTOR is linked to glioblastoma.