In the inflammatory-immunological process that is characteristic of dysbacteriosis and that can cause CRC, activation of the NF-κB pathway occurs, and this then causes conformational changes in the neoplastic environment, stimulates action of the pro-inflammatory cytokines, such as IL6, which has an important pathogenic role in the progression of CRC and regulates genes related to the tumor necrosis factor (TNF) and COX-2 enzyme, both highly expressed in neoplastic conditions (66). The gene discussed is TNF; the disease is colorectal carcinoma.