From a therapeutic perspective, the Akt-mTOR-S6K pathway is dysregulated in multiple animal models of monogenic causes of ASD including fragile X mental retardation [108], Rett syndrome [109] and tuberous sclerosis [110], whereas IGF1 ligands may improve neurodevelopmental symptoms in Rett [111] and the SHANK3 autism-related mouse model of Phelan-McDermid syndrome [112]. Here, SHANK3 is linked to tuberous sclerosis.