Given our findings that the HJURP levels were increased and that this protein resides in the same complex with PRDX1 in PCa cells, we hypothesized that the increase in the number of HJURP proteins leads to more disulfide-linked intermediates formed with PRDX1, attenuating PRDX1 hyperoxidation, promoting PRDX1 recycling, and ultimately enhancing PRDX1 peroxidase activity. This evidence concerns the gene PRDX1 and posterior cortical atrophy.