Given the similar network dynamics observed in Fmr1 rodent models [5, 7, 14, 44], findings reported here may not only extend mouse model concepts to FXS patients, but suggest that neurophysiological measures may be useful for tracking this local circuit deficit in both mouse models and patients to foster direct translational drug development for this neurodevelopmental disorder. This evidence concerns the gene FMR1 and neurodevelopmental disorder.