One factor that could be contributing to this deficit is the dysregulation of translational responses induced by excessive mGluR activation (Muddashetty et al., 2007), disruption of PSD-95 and CAMKII activities (Zalfa et al., 2007) and/or by the abnormal morphology of dendritic spines seen in FXS (Comery et al., 1997; Bilousova et al., 2009). This evidence concerns the gene DLG4 and fragile X syndrome.