Tuberous sclerosis complex (TSC) is a disorder characterized by the formation of benign tumors, intellectual disability, epilepsy, infantile spasm, and ASD (Smalley et al., 1992). Heterozygous mutations in either TSC1 or TSC2 genes that encode the proteins hamartin and tuberin, respectively, are sufficient to cause TSC (van Slegtenhorst et al., 1997; European Chromosome 16 Tuberous Sclerosis Consortium, 1993). Hamartin and tuberin form a heterodimer that negatively regulates the mTORC1 (mammalian target of rapamycin complex 1) signaling cascade by inactivating the small G protein Rheb (Tee et al., 2003). The mTORC1 signaling cascade has been implicated in cell growth and proliferation (Fingar et al., 2002) and in synaptic plasticity (Hoeffer and Klann, 2010).
