In fact, ASD-like behaviors and altered synaptic functions, similar to the symptoms observed in FXS model mice [28], were generated in mice, either by the overexpression of eIF4E [29] or by genetic deletion of eIF4E-binding protein 2 (4EBP2) [30], which is the major 4EBP species produced in neuronal cells [31] that inactivates eIF4E function by blocking eIF4F complex formation [20,32,33]. This evidence concerns the gene EIF4E and fragile X syndrome.