We also showed that the synergistic effect of LPS and TGF-β1 (0.1 ng/ml) in upregulating vimentin expression and downregulating E-cadherin expression was abrogated by the TLR4 inhibitor CLI-095, demonstrating that LPS-mediated TLR4 activation plays a crucial role in augmenting the TGF-β dependent EMT response in BPH-1 cells. This evidence concerns the gene TLR4 and benign prostatic hyperplasia.