In a second subtype of AR-expressing prostate cancer cells derived from castrated patients (e.g., LNCaP, LAPC-4, MDA-PC-2B, VCAP, etc), the cells have developed castration resistance mechanisms (i.e., mutation, gene amplification, protein over-expression) to activate AR signaling for their continued growth even in the presence of castrate levels of androgen [7]. This evidence concerns the gene AR and prostate carcinoma.