Thereafter, free NF-κB was dissociated from the complex and then translocated into the nucleus to activate related target genes, ultimately leading to the overexpression of a variety of proinflammatory cytokines, such as cyclooxygenase (COX-2), inducible nitric oxide synthase (iNOS), IL-6 and TNF-α, which promoted the occurrence and development of intestinal inflammation [64,65]. This evidence concerns the gene NOS2 and gastroenteritis.