Increased Akt/mTOR activity is consistent with deficiencies of FMR1, TSC1/2, or PTEN found in Fragile X, TSC, and Cowden syndrome and suggests that increased Akt/mTOR activity may have a role in the pathophysiology of the general ASD population and not limited to single ASD genetic mutations. The gene discussed is AKT1; the disease is Cowden disease.