In addition to creating a tumor-favorable microenvironment consisting of various tumor-promoting inflammatory cells (7), NF-κB-mediated inflammation has now been demonstrated to enhance the tumorigenic potential of cancerous cells through upregulation of Wnt/β-catenin signaling, further strengthening the idea that NF-κB may be an attractive therapeutic target for inflammation-associated cancer. This evidence concerns the gene NFKB1 and inflammatory response.