Our results indicate that LEDGF/p75 overexpression attenuates oxidative stress-induced necrosis but not STS-induced apoptosis in PCa cells, consistent with our previous observation that this protein is cleaved during apoptosis by caspase-3 into a p65 fragment that lacks stress survival activity and accelerates cell death [22,23,30]. The gene discussed is CASP3; the disease is posterior cortical atrophy.