Collectively, these findings: i) directly demonstrate that the EGFR is significantly more activated in PSC cholangiocytes compared to normal liver and other liver diseases; ii) indirectly support the concept that cholangiocytes may contribute to the biliary inflammation and fibrosis observed in PSC, and iii) demonstrate that LPS can induce EGFR phosphorylation and proliferation in an animal model of hepatic injury. The gene discussed is EGFR; the disease is liver disorder.