Although a few studies have demonstrated that de-repressed miR-122 targets, e.g., KLF6, P4HA1 and TGFBR1 could promote liver fibrosis [15,27,51], the mechanisms of how hepatocyte—produced miR-122 could regulate HSC and whether these miR-122 downstream molecules could serve as a therapeutic target for liver fibrosis are still not clear. This evidence concerns the gene KLF6 and Hepatic fibrosis.