At CRPC stage, the cancer cells bypass their dependency on the androgen signaling by various mechanisms such as somatic mutations or amplification of AR gene, constitutively active splice variants (AR-V7 and ARv567es), mutations in the ligand binding domain of AR (F877L and T878A), or activation of androgen-regulated genes via glucocorticoid receptor (Taplin et al., 1995; Arora et al., 2013; Antonarakis et al., 2014). This evidence concerns the gene AR and cancer.