In the United States 3.5 million individuals currently suffer from chronic hepatitis C virus (HCV) infection, and the incidence of new cases of acute infection has increased dramatically over the past few years. This is of significant concern because HCV infection often leads to liver cirrhosis and hepatocellular carcinoma (HCC), conditions that permanently hinder liver function and can result in liver failure. Liver fibrosis is the intermediary wound healing process that occurs prior to the onset of both liver cirrhosis and HCC. Unlike cirrhosis and HCC, liver fibrosis is reversible. Activated STAT3 protein, pSTAT3, can mediate the expression of immune genes and has been previously shown to alter the proliferation of cancer cells. Our study investigated the role and association between miR-30c, a molecule involved in transcriptional regulation, and pSTAT3 in HCV infected human hepatocytes. Following HCV infection, it was found that there was a decrease in pSTAT3 expression and cell proliferation. Moreover, upon miR-30c transfection of HCV infected human hepatocytes, there was found to be an even greater decrease in pSTAT3 expression and cell proliferation. This signifies that miR-30c may serve an anti-fibrotic role by reducing pSTAT3 expression, leading to greater inhibition of HCV induced cell proliferation. These observations are significant because they may pose a novel pathway for the development of anti-fibrotic clinical therapies.