 Therefore, the cancer risk posed by PhIP depends on the extent at which PhIP is metabolized.After absorption, PhIP is converted to a genotoxic metabolite in the liver by Phase I enzyme N-oxidation by Cytochrome P-450 1A2 (CYP1A2).PhIP can be further metabolized into a more potent metabolite through O-acetylation by hepatic or colonic N-acetyltransferase 1 (NAT1) and N-acetyltransferase 2 (NAT2), or by sulfotransfereases.