In different animal models, as well as various liver diseases, the progression of liver fibrosis is associated with significant hepatocyte injury and the release of various profibrotic factors, including transforming growth factor-beta (TGFβ), connective tissue growth factor, tissue inhibitors of metalloproteinases (TIMPs), and interleukin 6 (IL-6), which are hypothesized to activate the surrounding HSCs in a paracrine manner (7, 8). This evidence concerns the gene IL6 and liver disorder.