Phosphorylation of p65 at Ser536 is also an indicator of NF-κB activation.13 Cross talk between β-catenin and NF-κB has a significant role in regulating the expression of their target genes.14, 15, 16 For example, p65 is recently reported to inhibit β-catenin binding on the positive cis element TCF-binding element0 (TBE0) site of the cyclin D1 promoter and thus its transcription.17 Therefore, NF-κB has attracted much attention as a novel regulator of the β-catenin/cyclin D1 pathway in colorectal cancer cells. This evidence concerns the gene CCND1 and colorectal cancer.