Interestingly, treatment of WT LP with cecal contents from Dok3−/− mice triggered an increased production of pro-inflammatory cytokines associated with pathogenesis of IBD such as IL-23, TNFα, and IL-1β [19–22], as compared to treatment with cecal contents from WT mice (Fig. 3A), suggesting that the dysbiotic microbiome from Dok3−/− mice is sufficient to drive colonic inflammation. The gene discussed is IL1B; the disease is inflammatory bowel disease.