Among those phenotypic alterations, it has been shown that rapamycin inhibited proliferation and protein synthesis in astrocytes [118,119] (Table 1), indicating that mTORC1 overactivation regulates astrocyte function in NF1 and is probably linked to glioma formation, such that pharmacological inhibition of mTORC1 suppresses tumor growth both in NF1 patients [140,141] and in mouse models [142,143]. The gene discussed is NF1; the disease is neoplasm.