EIF4E and fragile X syndrome: Finally, and perhaps most importantly, a direct role for overactivated mTORC1 signaling in ASD core symptoms is supported by multiple evidence in mouse models of TSC [77,87,88], PTEN-ASD [100], FXS [160,166] and eIF4E-NS-ASD [49,50], showing that pharmacological or genetic inhibition of mTORC1 cascade both upstream and downstream of its kinase activity rescues or attenuates ASD-relevant behaviors, highlighting the potential therapeutic value of drugs targeting this pathway for patients.