A major single-gene cause of autism is fragile X syndrome (FXS), a developmental disorder associated with intellectual disability and a high incidence of epilepsy. FXS develops due to silencing of the FMR1 gene and subsequent loss of FMRP, a potent repressor of translation. The long-term depression of synaptic strength (LTD) induced by metabotropic glutamate receptor 5 (mGluR5) activation is enhanced in the FXS mouse model (Fmr1 KO), and it has been suggested that the protein synthesis downstream of mGluR5 significantly contributes to the synaptic pathophysiology of the disorder. Consistent with this, we find that hippocampal protein synthesis is excessive in the Fmr1 KO, and that acute pharmacological inhibition of either mGluR5 or the ERK1/2 signaling pathway is sufficient to normalize protein synthesis to WT levels. This correction is specific to the ERK1/2 pathway, as inhibition of the mTOR pathway does not normalize protein synthesis in the Fmr1 KO. Interestingly, it had been shown that a mild reduction of ERK1/2 activity can be achieved by disrupting the posttranslational maturation of the upstream activator, Ras using the HMG-CoA reductase inhibitor, lovastatin. Based on these findings, we tested the efficacy of lovastatin for correcting pathological phenotypes in the Fmr1 KO. Remarkably, we find that lovastatin, a drug in widespread use and approved to treat hypercholesterolemia in children, decreases Ras-ERK1/2 signaling, normalizes excessive protein synthesis, corrects exaggerated hippocampal mGluR-LTD, eliminates hippocampal epileptiform activity, normalizes neocortical hyperexcitability, and significantly ameliorates audiogenic seizures (AGS) in the Fmr1 KO mouse. These data suggest that lovastatin is potentially disease modifying, and could be a viable prophylactic treatment for FXS.