Considering the importance of the level of FMRP protein in the modulation of clinical phenotypes of FXS and its role as a modulator of translation by binding to target mRNAs, we first hypothesized that drugs that have the potential to normalize the altered gene expression profile in fmr1 KO mice or FXS patients may alleviate the neurobehavioral deficits seen in fmr1 KO mice. This evidence concerns the gene FMR1 and fragile X syndrome.