Perhaps more relevant to our experimental model of a biliary disease (biliary atresia), only miR-30b/c, -200b, -204 and −320 have been reported to change their expression levels in cholangiocarcinoma tissues or cell lines, [10,25-28] with miR-30 family members increasing in lipopolysaccharide-induced NFκB activation in cholangiocytes and after Cryptosporidium parvum infection, and being required for hepatobiliary development [10,25,26]. The gene discussed is NFKB1; the disease is biliary atresia.