After ingestion, AFB1 is activated by cytochrome P450 within the liver microsome system to produce large amount of toxic metabolite.28, 29 HBV infection has been reported to facilitate metabolism and bioactivation of AFB1 in the liver via the transactivation of pregnane X receptor (PXR) and induction in CYP3A4.30, 31 Moreover, HBV originating from chronic hepatitis or the virus itself could exacerbate host response to AFB1 and down‐regulated detoxification‐related proteins,32, 33, 34 making HBV‐infected hepatocytes more susceptible to AFB1 toxicity. The gene discussed is CYP3A4; the disease is chronic hepatitis.