NFE2L2 and glaucoma: Experimental studies have reported that the rise in ROS starts immediately after an increase in IOP, which in turn induces an endogenous antioxidant defense system via a nuclear factor erythroid 2-related factor 2 (NRF2) pathway.[19] Meanwhile, if elevated IOP induces the oxidative pathways and causes ROS and other mediators to both initiate and sustain neuroinflammation in glaucoma, the question arises as to why most eyes with OHT remain damage-free or at least maintain a healthy optic disc for considerably longer periods.