To examine whether co-targeting androgen and c-Met signaling pathways could effectively impede the progression of prostate cancer, we initially demonstrated the feasibility and effectiveness of the c-Met inhibitor on repression of the proliferation of prostate cancer cells in a xenograft mouse model using an orally bioavailable c-Met small molecule inhibitor, PF-2341066 [11,20,21]. This evidence concerns the gene MET and prostate carcinoma.