Our quantitative proteomic data are in keeping with altered enzymatic activity in the liver disease patients, e.g., lower (40%) chlorzoxazone (CYP2E1 substrate) metabolic ratio in patients with moderate–severe liver disease, significantly (69%) lower caffeine (CYP1A2 substrate) metabolic ratio in decompensated liver disease (Pugh score ≥6), and no effects on the drug pharmacokinetics of the compensated disease (Pugh score =5) [10]. The gene discussed is CYP1A2; the disease is liver disorder.