Among many possible mechanisms, there are four ways by which androgen independence is attained in prostate cancers through modification of the AR status or function: a) overexpression of functional AR, b) AR mutation resulting in hyper-responsiveness to androgens, c) activation by nonandrogens (loss of ligand specificity), or d) activation of ligand-independent AR signaling pathways (Deutsch et al. 2004). Here, AR is linked to prostate cancer.