IBD-associated inflammation has the potential to mediate clonal evolution over time, by mechanisms of induced by oxidative stress, inflammatory chemokines and cytokine (IL-6, STAT3, TNF-α, IL-10, IL-12 and IL-23) hyperproduction that affect numerous metabolic processes involved in cell repair, eventually creating a microenvironment that provides a selective advantage to those clones able to more rapidly repopulate the healing mucosa and to survive a cytotoxic inflammatory insult [119,130]. The gene discussed is TNF; the disease is inflammatory bowel disease.