We previously reported that glutamate/aspartate transporter (GLAST)-deficient (GLAST−/− and GLAST+/−) mice show spontaneous RGC death and glaucoma-like optic nerve degeneration without developing elevated IOP.5, 6 The GLAST protein is essential for maintaining the extracellular glutamate concentration below neurotoxic levels7 and for regulating glutathione levels in Müller glia by transporting glutamate,8 the substrate for glutathione synthesis, into the cells. Here, SLC1A3 is linked to glaucoma.