Moreover, increased permeability due to tight cell junctions disruption found in SIBO patients can lead to the translocation of bacteria and their products, such as endotoxins, while endotoxemia further induces CD14 mRNA and nuclear factor kappa B (NF-kB) expression that consequently activates Toll-like receptor 4 (TLR-4) and stimulates the production of proinflammatory cytokines such as tumor necrosis factor α (TNF-α), IL-1β, IL-6, and IL-8 [31,34,35,46]. The gene discussed is NFKB1; the disease is serum lipopolysaccharide activity.