Androgen/AR signaling affects initiation and progression of BPH by altering expression of various growth factors in a paracrine and autocrine manner; these factors promote growth of prostatic epithelial and stromal cells, accompanied by increasing expression of epithelial-mesenchymal transition (EMT)-related molecules such as TGF-β, ZEB-1, and Snail [9, 10]. This evidence concerns the gene AR and benign prostatic hyperplasia.