Contrary to FXS, the pathophysiological bases of the disorders associated with FMR1 premutation appear to be related to a significant increase in FMR1 transcript [28], which has been suggested to cause a toxic gain-of-function effect due to mRNA–protein interactions that lead to aberrant protein synthesis and sequestration in the cytoplasm [29,30,31]. This evidence concerns the gene FMR1 and fragile X syndrome.