Some such therapies have targeted the γ-aminobutyric acid (GABA) neurotransmitter signaling pathway, based on evidence of GABAergic deficits in Fmr1 knockout (KO) mice (Gantois et al. 2006; Adusei et al. 2010; Paluszkiewicz et al. 2011), a rodent model with strong construct validity for FXS. Here, FMR1 is linked to fragile X syndrome.