Studies of mouse and other animal models have implicated various signaling pathways and molecules in the pathophysiology of FXS, including metabotropic glutamate receptor 5 (mGluR5, encoded by Grm5), γ-aminobutyric acid receptor A (GABAA), matrix metallopeptidase 9 (MMP9) and glycogen synthase kinase 3 β (GSK3β, encoded by Gsk3b). This evidence concerns the gene MMP9 and fragile X syndrome.