Further, the disruption of mGluR5-Homer resulted in phenotypes of FXS including reduced mGluR5 association with the postsynaptic density, deficits in agonist-induced translational control, protein synthesis-independent LTD, neocortical hyperexcitability, audiogenic seizures, and altered behaviors, such as anxiety and sensorimotor gating [68]. The gene discussed is GRM5; the disease is fragile X syndrome.