Glaucoma is a group of progressive optic neuropathies that lead to irreversible loss of retinal ganglion cells (RGC); the disease can be characterized by several symptoms with a common feature of the visual field loss. Until now, various risk factors of glaucoma development have been identified, but the detailed biological basis of this disease has remained unclear. It has been postulated that the efficiency of cellular endogenous neuroprotective systems can be one of crucial factors affecting the RGC’s apoptotic susceptibility. More recently, in vivo evidences revealed that changes in HuR subcellular localization within RGCs occurred at early times after IOP induction in an animal model of glaucoma; these effects were followed at longer times by a progressive decrease of cytoplasmic HuR levels, including the expression of proteins essential for cell homeostasis (p53, Hsp70) and likely contributes to chronic IOP‑induced RGC degeneration. Similar alterations in HuR content and subcellular localization were found in human POAG samples, in support of the involvement of HuR in glaucoma. The potential of HuR as a new pharmacological target is shown by an increasing interest in medicinal chemistry by the field. The role of post‑transcriptional mechanisms controlling gene expression in glaucoma, needs to be further explored.