In addition to the disrupted excitation/inhibition (E/I) balance in various ASD models (which may be a consequence of defective homeostatic plasticity) [69,70], defective homeostatic synaptic plasticity has been directly examined and reported in Mecp2 KO (a Rett syndrome model) [66,67,71], Fmr1 KO mice [29,30], and FXS human neurons [31]. This evidence concerns the gene FMR1 and fragile X syndrome.