BBR is primarily metabolized and eliminated by liver CYP2C9 (analogous to Cyp2c29 in mice).[20] Our in vivo pharmacokinetic profile assays, liver S9 enzyme kinetics, and primary hepatocyte studies revealed that hepatic steatosis‐induced reduction in CYP2C9 substantially decreased BBR clearance, leading to drug accumulation and delayed metabolite formation. This evidence concerns the gene CYP2C9 and fatty liver disease.