Sequential accumulation of somatic mutations and clonal expansions occur in IBD-associated CAC patients [27] and the chronic inflammatory microenvironment spurs the accelerated epithelial cell turnover by maintaining high concentration of inflammatory cytokines, such as IL-6, TNF-α and CXCL2, and the continued exposure to oxidative stress promotes neoplastic transformation of colon tissues [28–30]. This evidence concerns the gene TNF and inflammatory bowel disease.