This apparent threshold is of great relevance to previous and ongoing efforts to reactivate the FMR1 gene [53,54,55], since reactivation in the absence of the ability to produce FMRP would not be a productive approach to the treatment of FXS; moreover, the production of expanded CGG repeat RNA would increase the risk of developing the late-onset neurodegenerative disorder, FXTAS [19]. Here, FMR1 is linked to fragile X syndrome.