The results showed that TGF-β1 markedly induced Smad2 phosphorylation and up-regulated the expression level of TGFBR2 and vimentin proteins but reduced E-cadherin expression (Figure 5C, lanes 2 and 3 vs. lane 1), suggesting that TGFBR2/Smad2 signaling mediates TGF-β1-induced EMT in PCa cells. The gene discussed is VIM; the disease is posterior cortical atrophy.