Although the detailed mechanisms underlying the phenotype in FXS remain to be characterized, it has been reported that the absence of FMRP may lead to dysregulation of MEK/ERK and phosphoinositide 3-kinase (PI3K)/mammalian target of rapamycin (mTOR)/glycogen synthase kinase-3-beta (GSK-3β) signaling pathways [14–17]. This evidence concerns the gene MTOR and fragile X syndrome.