Correspondingly, Mdr2−/− and bile duct ligated mice, both models of cholestatic liver injury, demonstrate an increase in expression of hepatic IL-17A and its receptor IL-17RA, and aggregation of IL-17–producing cells in periductal areas.24, 30 In addition, other studies have reported a decrease in hepatic neutrophil accumulation, liver fibrosis, and liver damage in IL-17A or IL-17RA knockout mice or by blocking IL-17A.24, 31, 32, 33, 34 These studies suggest an injurious role for IL-17 signaling in cholangiocytes and cholestatic liver injury. The gene discussed is IL17RA; the disease is Hepatic fibrosis.