These findings are consistent with recent reports for other drug-metabolizing enzymes (e.g., CYPs, NAT1) [41], and support a hypothesis that intratumoral expression of UGTs and other drug-metabolizing enzymes can impact cancer patient survival through not only drug metabolism but also metabolism of numerous endogenous bioactive molecules (e.g., steroid hormones, amino acids, fatty acids, bile acids) that can modulate cancer growth as briefly discussed below. This evidence concerns the gene NAT1 and cancer.