These findings suggest that the pathophysiology associated with the loss of FMRP or MeCP2 may not arise from irreversible developmental brain abnormalities, but result from functional disturbances of neural circuits that could be corrected in adulthood, providing a potential rational basis for treatment of neurodevelopmental disorders in adulthood (Castrén et al., 2012; Wijetunge et al., 2013; Hagerman et al., 2014). Here, FMR1 is linked to neurodevelopmental disorder.