The preclinical research conducted over the past 20 years has mainly focused on the excitatory glutamate transmission mediated by group 1 (Gp1) metabotropic glutamate receptor (mGluR1 and mGluR5) and the γ-aminobutyric acid (GABA) related inhibition to link the lack of FMRP to the mechanisms underlaying FXS physiopathology (Figure 3). The gene discussed is FMR1; the disease is fragile X syndrome.