Current treatment for patients with low-risk PCa is satisfying, but some subpopulations of tumor cells in progressive PCa can alter their nuclear androgen receptor expression levels and function through androgen receptor (AR) increase and hypersensitivity, AR mutations, co-activator/co-inhibitor mutations, androgen non-dependent AR activation and intratumoral androgen production, allowing cancer to survive with low androgen levels or in the absence of androgens (i.e., as CRPC) [145], making conventional therapies, particularly ADT, less effective. The gene discussed is AR; the disease is posterior cortical atrophy.