MiR-19a was correlated with advanced hepatic fibrosis in serum exosomes from HCV patients and, in HSC, directly stimulated fibrotic gene expression and inhibited SOCS3 expression via downstream activation of the STAT3/TGF-β1/Smad3 axis, the latter also occurring in response to exosomes from HCV-infected hepatocytes [255]. The gene discussed is TGFB1; the disease is Hepatic fibrosis.