Gain-of-function mutations in the Catenin Beta 1 (CTNNB1) gene, which are more prevalent in metastatic disease (4.3–5.4%) than in primary tumors (1.8–2.6%), cause hyperactivation of the Wnt pathway by stabilizing the β-catenin protein, thereby promoting an aggressive clinical course and resistance to both chemotherapy and AR inhibitors [10]. Here, CTNNB1 is linked to metastatic neoplasm.