In addition to supporting virus replication, our results suggest that virus-induced PEMT could orchestrate hepatic steatosis in people with hepatitis C. We showed that knocking down PEMT in HCV-infected cells reduced the amount of lipid and reversed virus-induced changes in SREBP 1-c, DGAT1 and MTP, proposed mediators of steatosis in hepatitis C [18,19,20]. The gene discussed is DGAT1; the disease is hepatitis C virus infection.