We recently showed that the expression of p65 and phospho-p65 was significantly elevated in bladder tumors, compared with corresponding benign urothelial tissues, and that the activity of NF-κB modulated by its activator or inhibitor was associated with urothelial tumorigenesis, using carcinogen-induced models (e.g., MCA in SVHUC cells, BBN in mice) [80]. This evidence concerns the gene NFKB1 and urinary bladder neoplasm.