A recent hypothesis for the emergence of ASD in TSC and related conditions is dysregulation of neurotrophic factors, including brain-derived neurotrophic factor (BDNF) which plays a role in protein regulation through inhibition of TSC1-TSC2 signaling and mutations in PTEN that lead to excessive mammalian Target of Rapamycin (mTOR) signaling. This evidence concerns the gene BDNF and tuberous sclerosis.