These results suggest that the upregulation of Nrg1 by glutamine-deprived Nf2−/− SCs occurs in a mTORC1-independent fashion, which could explain the cytostatic and heterogeneous clinical efficacy of mTORC1i in human patients, as well as the ‘rebound’ tumor growth that is often seen upon cessation of mTORC1i treatment and could be triggered by a reservoir of accumulated Nrg164, 65. Here, NF2 is linked to neoplasm.