In fact, in vivo studies reveal that mesenchymal markers (vimentin and S100A4) and Snail are expressed but CK19 and E-cadherin are not in cholangiocytes lining the remnants of extrahepatic bile ducts and peribiliary glands of biliary atresia [91, 94], suggesting that the occurrence of EMT in cholangiocytes is associated with an incomplete induction of apoptosis caused by the biliary innate immune response and that these surviving cells play a role in the sclerosing cholangiopathy of biliary atresia without inducing tolerance until the clearance of the virus. The gene discussed is SNAI1; the disease is biliary atresia.