Finally, both reports by Oushy et al. and Hallal et al. similarly suggested that pathways including ERK, mammalian target of rapamycin (mTOR), mitogen-activated protein kinases (MAPKs), AKT and c-Jun N-terminal kinases (JNKs) could underlie the effects of GBM–EVs on astrocytes (Fig. 3) [17, 36]. This evidence concerns the gene MTOR and glioblastoma.