Considering the facts that individuals with Inflammatory bowel disease (IBD) have a 10- to 40-fold increased risk of developing colorectal cancer compared with those without IBD [23] and that chronic persistent inflamed mucosa progresses through dysplasia to adenocarcinoma, known as the “inflammation-dysplasia-carcinoma sequence” in contrast to the “adenoma-carcinoma sequence” of sporadic colorectal cancer, earlier or continuous intervention with an anti-inflammatory agent targeting the inhibition of COX-2 and redox sensitive NF-κB can be an effective way to reduce or prevent CAC [24]. Here, PTGS2 is linked to dysplasia.