We propose that in castration-refractory prostate cancer cells, the colocalization of both AR and β-Catenin enables the AR to signal through the Wnt/β-Catenin signaling pathway, leading to a propagation of the already accelerated cell growth and an increased state of malignancy compared with the cells that only have one of the two aberrant signaling pathways (Figure 7D). Here, AR is linked to prostate carcinoma.