The chronic inflammatory bowel diseases (IBD), such as Crohn's disease (CD) and ulcerative colitis (UC), are multifactorial pathologies. There is overwhelming evidence that genetic factors play a pivotal role in the predisposition to suffer from IBD. The severity of the inflammatory response depends on genes coding for proteins which regulate the cytokine production. Among them, NF kappa B stands out as the most important regulator of the gene expression of several pro- and anti-inflammatory genes. We present hereby its structure, function, regulation and the role played in IBD. Different theories relating the mechanism of action of glucocorticosteroids to NF kappa B are described in this review as well. The more accurate knowledge of the NF kappa B physiology has allowed new therapeutical approaches to inflammatory diseases to appear, namely the transfer to primary intestinal epithelial cells by an adenoviral vector of a mutant I kappa B (the inhibitory protein of NF kappa B) and the local use of p65 antisense phosphorothioate oligonucleotides.