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Glaucoma, an ocular surface disease? Apparently not, if we only consider trabecular degeneration, IOP increase and ganglion cell death. However, instillations of eye drops for decades, especially when several drugs are needed and/ or in sensitized patients may induce conjunctival and ocular surface changes that may cause major issues over the long term, in particular at time of surgery. Many reports, in humans, animal or cell models confirmed that mild symptoms or signs may account for subclinical inflammatory changes impairing the tear film, eyelids, conjunctiva or cornea. One major component responsible for those findings is the preservative benzalkonium chloride, which is cytotoxic and has detergent properties. The study by Okada et al. (1462) is an experimental study evaluating the expression of stress-related genes c-fos and c-jun, and their corresponding encoded proteins activator protein(AP)-1 and cyclooxygenase (COX)-2 in rat cornea, a short time after instillation of antiglaucoma drugs or preservative. As early as 30 to 60 minutes after instillation, genes were upregulated, whereas AP-1 and COX2 were induced 90 minutes after instillation. These effects were more prominent with prostaglandins and benzalkonium at a 0.02% concentration. This study used a well validated set of complementary techniques to assess these results. Although experimentally performed in animal eyes, they showed that preserved drugs and prostaglandins may very quickly stimulate stress-induced signals in the ocular surface epithelia and they support similar studies in humans, especially in patients treated over the long term. Such data are quite consistent with previous reports showing overexpression of inflammation- or apoptosis-related markers in impression cytology specimens or conjunctival biopsies. This is a new example illustrating the involvement of the ocular surface in glaucoma and the noxious role of preservatives in corneal and conjunctival epithelia.