With advancing age, the exposure of the eye to various stressinducing factors increases, which can damage the integrity of the trabecular meshwork. These majorly include free radicals, reactive oxygen species and protein aggregation, which elevate oxidative stress in the eye. In PEXG and POAG the damage due to oxidative stress can also succumb into mitochondrial damage and neuronal death of retinal ganglion cells eventually leading to vision loss. BIRC6 is ubiquitin D-Pantothenic acid sodium carrier protein involved in the protection of the cell against apoptosis and reduces cellular stress. Increased intraocular pressure, ROS and free radicals create a stressful environment in the eye. In the ER, stress can be accompanied by the aggregation of misfolded proteins. The accumulation of misfolded proteins can activate a cytoprotective signal response known as unfolded protein response, which triggers the activator functions like adaptation, alarm and apoptosis. When stress is prolonged and adaptation and alarm fail to pull the cell back to normal condition, the UPR results in activation of apoptosis and also elicits an inflammatory response in order to restore the normal environment of the cell. This mechanism has been found to be involved in the pathogenesis of many neurodegenerative disorders like Alzheimer’s disease, Parkinson’s disease and cerebral ischemic insults. In PEXG and POAG the damage due to oxidative stress can succumb into mitochondrial damage. The extracellular matrix of the trabecular meshwork is disrupted as a consequence of damage to the mitochondria, a characteristic mechanism involved in the pathogenicity of POAG and PEXG. Konstas et al. have observed excessive mitochondrial alterations in PEXG. The highest level of 
mitochondrial damage and mitochondrial loss per cell was seen in PEXG as compared to POAG, which justifies its more aggressive nature. Zenkel et al have reported differential expression of ECM proteins and stress response genes in eyes of PEXG patients compared to eyes of normal healthy controls. The expression of ECM genes is upregulated, resulting in aggregation of ECM proteins. Glutathione S-transferase 1, which is involved in protection from oxidative stress, is downregulated. In addition, clusterin, an efficient extracellular chaperone, is downregulated in PEXG eyes, resulting in aggregation of pathologic ECM proteins. Consequently, abnormal proteins accumulate, resulting in the formation of pseudoexfoliative material. In the anterior chamber this Lomitapide Mesylate hinders the outflow of aqueous humor by clogging the trabecular meshwork, which results in elevation of the IOP. All these stresses succumb in severe degenerative changes in PEXG. Apoptosis might be one of the various mechanisms that is involved in the degeneration of retinal ganglion cells in PEXG. BIRC6 is an anti-apoptotic protein, which promotes cell survival by inhibiting caspases. Downregulation of BIRC6 by various polymorphisms and mutations leads to upregulation of p53, resulting in mitochondrial-mediated apoptotic cell death. As a consequence of stress, cytochrome C is released from mitochondria, which activates caspases and thus resulting in the degeneration and death of the cells. Recent GWAS studies by Nakano et al., for the Japanese population, Gibson et al., for British population, Ramdas et al., Dutch population have shown few loci and SNPs to be associated with Glaucoma but these studies did not find any association of the BIRC6 gene.