FMR1 and fragile X-associated tremor/ataxia syndrome: The origin of pathology in FXS and in some FPM carriers, with or without FXTAS mutations, is the presence of a CGG repeat expansion on FMR1, raising the possibility that some of the same molecular pathways could be affected in both disorders, and those associated with glutamatergic signaling in particular [1,74,90,91].