With regard to CRC, although a previous meta-analysis indicated that the NAT1 genotype was not significantly associated with an elevated CRC risk (Liu et al., 2012), a further study has demonstrated that in vivo knock-down of NAT1 in the HT-29 COAD cell line promoted an up-regulation of E-cadherin and cell–cell contact growth inhibition, thereby indicating that NAT1 may be a novel drug target for CRC therapeutics (Tiang et al., 2011). This evidence concerns the gene NAT1 and colorectal carcinoma.