The ‘mGluR theory’ of FXS, which is strongly supported by several lines of evidence, states that mental impairment and phenotypic behaviors associated with FXS arise, at least in part, from constitutive activation of translational pathways normally controlled by group 1 metabotropic glutamate receptor (mGluR1 and mGluR5) activity [9]. This evidence concerns the gene GRM1 and fragile X syndrome.