Despite these limitations to developing LDL-R as a target to block HCV infection, it is well-established that lipid abnormalities typical for chronic HCV infection, such as hepatic steatosis and hypocholesterolemia [118], would implicate high hepatic LDL-R levels, and accordingly, low PCSK9 levels in chronic HCV. This evidence concerns the gene LDLR and Hepatic steatosis.