For activated TGF-β/Smad signaling is an important pathophysiological basis of BPH, first, we treated BPH-1 cells and WPMY-1 cells exposed to TGF-β1 with 25-OH D. We revealed that 25-OH D could significantly suppress the phosphorylation of Smad2 and Smad3, and thereby restrained the transcriptional activity of Smad2/Smad3/Smad4 complex induced by TGF-β1 in both BPH-1 cells and WPMY-1 cells (Figures 1(a)–1(d)). This evidence concerns the gene SMAD4 and benign prostatic hyperplasia.