Based on the latest research data implying that ER stress and activation of the PERK-dependent UPR signaling pathway may be closely correlated with POAG pathogenesis at the molecular level, the main aim of the present study was to evaluate the effectiveness of the small-molecule PERK inhibitor LDN-0060609 in an in vitro cellular experimental model of glaucoma, since targeting of the components of the UPR signaling branches may contribute to the development of an innovative, ground-breaking treatment strategy against POAG. Here, EIF2AK3 is linked to open-angle glaucoma.