The mechanisms underlying ERp57 upregulation in prostate tumor tissues are not clear, but it is plausible that the high metabolic rate of PCa cells, combined with the pro-inflammatory prostate tumor microenvironment, increases oxidative stress leading to upregulation of stress and antioxidant defense proteins such as LEDGF/p75 and its target genes [68]. This evidence concerns the gene PROS1 and posterior cortical atrophy.