NFKB is constitutively inactivated and its activation, with subsequent immuno-inflammatory response alteration, may be due to a dysregulation in the ubiquitin–proteasome system, which is a mechanism of intracellular protein degradation, occurring in atherogenesis, neurodegenerative and autoimmune diseases, and, possibly, in IBD and CRC [41,42]. This evidence concerns the gene NFKB1 and inflammatory bowel disease.