A trough concentration of 3.0 mg/L is associated with increased hepatotoxicity, particularly in the Asian population, and 4.0 mg/L is associated with increased neurotoxicity.[20] Blood concentration of VRCZ can be affected by several factors, including patients’ age, race, drug–drug interactions, route of administration, and cytochrome P450 (CYP) polymorphism, predominantly CYP2C19.[17,21–27] VRCZ is mainly metabolized in the liver by cytochromes CYP2C9, CYP 3A4, and CYP2C19.[28] Therefore, the capacity of VRCZ metabolism by the liver is attenuated in patients with liver failure. This evidence concerns the gene PPIG and liver failure.