Although the present study does not present proinflammatory cytokines plasma concentrations for the investigated participants, the reduction in the in vivo activity of OCT1/2 observed in patients with severe stages of liver fibrosis and cirrhosis after achieving sustained virologic response (Phase 2) may be related to the inflammatory response in chronic HCV infection, in addition to the fibrotic process, which can also alter OCT1/2 transporter activity [18,43,44,45]. The gene discussed is SLC22A1; the disease is Cirrhosis.