In our study, the intrahepatic expression of TGFB1 was approximately four times higher in HCV carriers than in controls; moreover, a significant increase in this gene was associated with the highest levels of necroinflammatory activity and high liver fibrosis scores, demonstrating that in chronic hepatitis, with the failure of the immune system to control viral replication, there is a persistent recruitment of mononuclear inflammatory infiltrate, leading to chronic inflammation with sustained liver damage that is modulated by several factors, including TGF-β1 and IL10 [29, 30]. The gene discussed is TGFB1; the disease is chronic hepatitis.