Based on Moriwaki data obtained in a mouse model of colitis, as well as in an experiment on bone-marrow-derived dendritic cells, it can be concluded that after LPS-induced stimulation of TLR4, RIPK-3 participates in the activation of the NF-κβ pathway, which leads to interleukin expression and STAT3 phosphorylation (Moriwaki et al., 2014). Here, NFKB1 is linked to colitis.