AR and posterior cortical atrophy: Many mechanisms for castration resistance have been proposed [5,7,8,9,10]: the continuous role of androgen receptor (AR) signaling in CRPC due to the amplification/mutation of ARs or the increased expression of AR splice variants or androgen synthesis enzymes in PCa cells [5,6,11]; the activation of other signaling transduction pathways that lead to either the enhanced activity of ARs and its coactivators or the bypassing of ARs in the presence of low levels or even in the absence of androgen [5,6,12]; and the existence of PCa stem cells that do not depend on ARs to survive [5,6].