Genetic polymorphisms resulting in lack of enzyme activity due to homozygous deletion of the GSTM1 and GSTT1 genes have been described.18 The frequencies of these deletions vary across populations.19 Molecular epidemiologic studies have shown increased risk for various cancers among individuals with the NAT1 rapid acetylator or NAT2 slow acetylator genotypes, in the presence of known carcinogen exposure, such as smoking or dietary exposure to heterocyclic amine.20 Here, NAT2 is linked to cancer.