Since increased TGF-β levels can increase the production of extracellular matrix proteins and their receptors and inhibit the synthesis of matrix-degradative proteolytic enzymes we postulate that HCV infection through the modulation of TGF-β signaling can promote immune evasion, viral persistence as well as induction of fibrosis leading to end stage liver disease. The gene discussed is TGFB1; the disease is liver disorder.