It is important to emphasize that while the increase in expression of AR splice variants such as ARv7, which can activate AR-mediated gene expression in the absence of ligands, has been shown to be one mechanism by which prostate tumor cells become resistant to anti-androgens and other hormone deprivation therapies (reviewed in [25]), we observed these effects of UGDH overexpression with no detectable increase in ARv7 or other splice variant expression. This evidence concerns the gene AR and prostate neoplasm.