In addition, inhibition of nuclear translocation of p52 and its interaction with AR by AR/p52-02 likely led to a decrease in AR transcriptional activity (as shown by a decrease in PSA mRNA) and growth inhibition of PCa cells under low androgen condition, which would be consistent with the findings of Nadiminty et. al, where p52 was found to activate AR via interaction at the NTD of AR, causing increased AR transcriptional activity and increased growth of PCa cells under androgen deprivation [10]. The gene discussed is NFKB2; the disease is posterior cortical atrophy.