In agreement with in vitro data showing that NLRP12 antagonizes NF-κB signaling pathways, NLRP12−/− mice were more susceptible to intestinal inflammation, colitis and the associated colorectal tumorigenesis, due to a failure to resolve pro-inflammatory non-canonical NF-κB, ERK, and AKT signaling, which resulted in elevated levels of pro-inflammatory cytokines and chemokines (Figure 5). This evidence concerns the gene NFKB1 and colitis.