The studies in hepatic impairment (accessed by Child–Pugh score) in HCV-negative patients with liver cirrhosis, hepatitis B infection, alcoholic liver disease, or previous HCV infection demonstrated an AUC increase in glecaprevir (a substrate of P-gp, BCRP, and OATP1B1/1B3, with about 28% of dose metabolized mostly by CYP3A4, minimal renal and some biliary excretion) (when co-medicated with pibrentasvir) in mild (by 33%), moderate (by 100%), and severe (1010%) hepatic impairment. Here, CYP3A4 is linked to hepatitis B virus infection.