Most commonly used mouse models of TSC, such as mice harboring heterozygous genetic deletions of Tsc1 or Tsc2, exhibit phenotypes that recapitulate aspects of the human disease, including synaptic dysfunctions, deficits in learning and memory, and impaired social interactions (Goorden et al., 2007; Ehninger et al., 2008; Sato et al., 2012; Tang et al., 2014). This evidence concerns the gene TSC1 and tuberous sclerosis.