Involvement of potential dysfunctions in lipid homeostasis in FXS is further suggested by the findings that HMG-CoA reductase inhibitors that reduce cholesterol synthesis partly correct pathological dysfunctions in Fmr1 KO mice [74] and decrease Gp1 mGluR signaling to ERK1/2 in Fmr1 KO null neurons [57], lending indirect support for a potential role of the cholesterol biosynthetic pathway in FXS manifestations, at least in animal models. The gene discussed is GTPBP1; the disease is fragile X syndrome.