By contrast, tumor cells can re-gain active AR signaling that is independent of androgen ligand-mediated activation of the AR by means of generating constitutively active splice variants of the AR (23–26), altering the mode of actions of the AR in a receptor-dependent manner (27), or by relying on the downstream signaling of other hormone receptor pathways, such as the glucocorticoid receptor (28). This evidence concerns the gene AR and neoplasm.