Our finding is of particular interest because in the present population the virus was not actively replicating, which led us to hypothesize that the role IL28B polymorphism plays in regulating the development of hepatic steatosis in HCV patients is not independent from, but presumably mediated by the poor control on HCV replication that patients with the unfavourable IL28B genotype exert and requires the presence of actively replicating HCV virus to be played. The gene discussed is IFNL3; the disease is fatty liver disease.