Several mechanisms for the castration resistance have been proposed, including the continuous role of AR signaling or the activation of other signaling transduction pathways in CRPC that lead to either enhanced activity of AR and its coactivators or bypassing AR in the presence of low levels or even in the absence of androgen [1, 2], the trans-differentiation of PCa stem cells into androgen-independent (AI) cell-types [1, 2], and the inflammatory signaling in both tumor microenvironment and in PCa cells that promotes the emergence of PCa castration resistance [14, 39, 40]. Here, AR is linked to neoplasm.