Genomic AR signaling in PCa is well studied: AR disassociates from its cytoplasmic chaperones such as HSP70 and translocates to the nucleus upon androgenic hormone binding, working as either homodimer or heterodimer to regulate its downstream genes such as PSA, FKBP5, and TMPRSS2, in order to provide survival signals for PCa growth (Figure 1; Smith and Toft, 2008). The gene discussed is FKBP5; the disease is posterior cortical atrophy.