Several mechanisms including amplification of the AR gene, upregulation of mRNA expression to allow binding by low levels of androgens, mutations in the ligand binding domain (LBD) that allow the receptor to be activated by antagonists, and alteration in the normal AR signaling pathway, have been proposed to explain the ability of prostate cancer to recur in the presence of androgen ablation therapy [33,34]. This evidence concerns the gene AR and prostate carcinoma.