In addition to natural and synthetic glucocorticoids (Chang et al. 2001), an AR with the T878A mutation was found to be activated by E2 and progesterone (Zhao et al. 2000), and PCa cells expressing one of the mutant ARs could obtain a growth advantage after cortisol exposure (Krishnan et al. 2002). The gene discussed is AR; the disease is posterior cortical atrophy.