We previously reported that interleukin-1-dependent activation of GLAST increases glutamate uptake by Müller glia and protects RGCs from excitotoxicity.11 In addition, glial cell line-derived neurotrophic factor and neuturin-induced upregulation of GLAST in Müller cells is required to protect RGCs following optic nerve transection.12 Therefore, discovering new compounds that enhance EAAT1 activity may represent a novel strategy for therapeutic management of glaucoma. This evidence concerns the gene SLC1A3 and glaucoma.