Moreover, silencing of other members of the NF-κB pathway, REL-A, transforming growth factor-activated kinase (TAK)1 or both IκB kinase (IKK)1 and IKK2, in IECs increased murine susceptibility to spontaneous colitis, providing a strong link among NF-κB activity, epithelial apoptosis, and intestinal inflammation [53–55]. Here, NFKB1 is linked to colitis.