Furthermore, recent evidence suggests that disruption of the SHANK3 and glutamate signaling pathway is common to multiple forms of ASD, including Fragile X syndrome and tuberous sclerosis [19,20]; dissecting this pathway may therefore represent an important opportunity to improve understanding of the biological pathways associated with ASD and ID not involving haploinsufficiency of SHANK3. This evidence concerns the gene SHANK3 and tuberous sclerosis.