The amplification or mutation of the AR gene [3] and the expression of truncated AR splice variants that display ligand-independent activity [4] have been linked to molecular mechanisms of resistance/response not only to anti-androgen drugs (such as abiraterone and enzalutamide), but also to other standard-of-care treatments for advanced PCa (such as taxols) [5]. Here, AR is linked to posterior cortical atrophy.