Guided by specific proteins, AR then translocates into the nucleus[4] and binds to androgen response elements (AREs) as homodimer on DNA.[5] Here the AF2 site recruits coregulators and other proteins to form a transcriptional regulatory complex.[2, 3, 6] Current strategies for the treatment of PCa typically involve inhibiting androgen synthesis (chemical castration) and blocking AR transcriptional activity.[7] The latter normally refers to antagonists which competitively bind to the AR‐LBP. Here, AR is linked to posterior cortical atrophy.