Results of pharmacokinetic studies are in part inconsistent (due to complexity of factors affecting drug kinetics in liver failure patients) with the present study findings; however, some could indicate reduced CYP3A4 metabolic capacity of the liver, i.e., increased steady-state exposure and Cmax of grazoprevir changing with the Child–Pugh class [53] or pibrentasvir (also a substrate for CYP1A2 down-regulated in the present study) AUC increase by 51%, 31%, and 5.2-fold in patients with the Child–Pugh A, B, and C, respectively [47]. Here, CYP1A2 is linked to liver failure.