As excessive tonic protein synthesis is a feature of FXS, and reversing this appears to rescue some of the fragile X disease phenotypes in mice and cultured cells, miRNAs may be playing a role similar to FMRP (indeed the two may be working together in this pathway, given the close interaction of FMRP with miRNA components, and the observation that phosphorylation of FMRP prevents its binding to dicer [52]). This evidence concerns the gene FMR1 and fragile X syndrome.