The predominant genetic and cellular changes in human prostate cancer include presence of the TMPRSS2-ERG gene fusion [3]; loss of the phosphatase and tensin homolog (PTEN) tumor suppressor gene leading to accumulation of its substrate phosphatidylinositol 3,4,5-triphosphate (PIP3) and constitutive PI3K-pathway up-regulation [4]; amplification, over-expression or mutation of the androgen receptor (AR) [2]; and amplification of the MYC oncogene [5], [6]. This evidence concerns the gene AR and prostate cancer.