Prostate cancer epithelial cells depend on androgens for their survival. Because of this dependence, androgen deprivation therapy is the major treatment of advanced prostate cancer. Such therapy is effective in delaying progression of the disease. However, inevitably with time, the tumors continue to grow. This stage of the disease is referred to as Castration Resistant Prostate Cancer (CRPC). A key question has been how CRPC can survive and then grow in the face of castrate levels of androgens. Dr. Tindalls laboratory has discovered a potential mechanism by which prostate cancer cells survive following androgen deprivation therapy. His laboratory team has shown for the first time that naturally occurring androgen receptor variants can support the expression of many endogenous androgen dependent target genes, as well as the growth of CRPC cells in the absence of androgens. These variants lack the androgen-binding-domain of the receptor protein and are constitutively active. Splice variants increase following androgen depletion and may play an important role in driving proliferation of cells in CRPC. This discovery provides important information to the pharmaceutical industry and may lead to new therapeutics for prostate cancer patients.