Considering that normal prostates contain high concentrations of zinc, and loss of zinc occurs during prostate carcinogenesis, the zinc-mediated blockage of androgen signaling by the downregulation of AR expression would appear to contribute to PCa cell proliferation; low levels of zinc during prostate carcinogenesis would increase AR expression and favor cell proliferation, and could therefore be one of the critical steps in transformation. The gene discussed is AR; the disease is posterior cortical atrophy.