As a consequence, in transfected cells, miR-27a/b determined the repression of both Peroxisome Proliferator Activated Receptor Alpha (PPAR-α), which led to triglycerides accumulation and Angiopoietin Like 3 (ANGPTL3), that caused an increase in lipoprotein lipase (LPL) activity and fatty acid uptake into hepatocytes, thus highlighting a possible mechanism contributing to a miR-27a/b mediated HCV-induced steatosis in patients [45]. This evidence concerns the gene ANGPTL3 and steatosis.