On the other hand, inactivation of the NFκB pathway has also been associated with increased inflammation: a) mice lacking Iκkβ expression in intestinal epithelial cells (IEC) show increased susceptibility to chemical-induced colitis[55]; b) mice lacking Iκkγ/Nemo, and without Nfκb activity in IEC develop spontaneous colitis[56]; c) ablation of Iκkγ in keratinocytes is associated with psoriasis in mice[57]; d) Iκkβ deletion causes progressive neutrophilia, with increased IL1β expression and loss of inflammasome down-regulation in Nfκb-deficient myeloid cells[58], [59], [60]. This evidence concerns the gene IL1B and colitis.