According to the mGluR theory of FXS, absence of FMRP regulatory control leads to increased protein synthesis and exaggerated metabotropic glutamate subtype 5 receptor (mGluR5) signaling, affecting relative glutamate and gamma-aminobutyric acid (GABA) levels creating excitatory–inhibitory neurotransmitter imbalance [2,3,4]. Here, FMR1 is linked to fragile X syndrome.