The discrepancy between the studies could be related to the reduced hepatocyte volume in the liver, and thus the diminished total liver CYP2C19 metabolic capacity developing with liver failure progression [18], as well as to a genetic status of the subjects (the patients of Adedoyin et al. [2], were phenotyped and poor metabolizers were excluded from the study, but as stated above apart from quantitative changes of the enzymatic protein abundance many other factors can affect pharmacokinetics in liver failure patients; our study excluded poor metabolizers of CYP2C19 and CYP2D6). This evidence concerns the gene CYP2C19 and liver failure.