In our previous study, we observed that capsaicin, a chili pepper component, down-regulated TCF4 without reducing the level of β-catenin protein and subsequently decreased β-catenin/TCF-dependent transcriptional activity in HCT116 adenocarcinoma human colorectal cancer cells, indicating that down-regulation of TCF4 is responsible for β-catenin/TCF-dependent transcriptional activity in capsaicin-treated colorectal cancer cells [16]. This evidence concerns the gene HNF4A and adenocarcinoma.