Although FMRP is generally considered a translation suppressor and increased mGluR1/5-dependent dendritic protein synthesis is largely due to the loss of FMRP in neurons in FXS [86], the observation that genetic or pharmacological inhibition of mGluR5 activation effectively and significantly reduces mGluR1/5-dependent dendritic protein synthesis in fmr1−/− mice [90,91] also implicates that mGluR1/5 activation is abnormally enhanced in FXS. Here, GRM1 is linked to fragile X syndrome.