The apparent opposite direction for phenotypic and genetic measures of acetylation statuses with bladder cancer risk may reflect dual functions of NAT2 in bladder carcinogenesis because the CMR only measures the systemic detoxification capacity through the hepatic N-acetylation pathway while the SNP-inferred NAT2 acetylation represents both hepatic detoxification and local carcinogen activation through the O-acetylation pathway at local urothelium. This evidence concerns the gene NAT2 and urinary bladder cancer.