This effect could be mediated through several pathways, including the upregulation of PPARγ, which acts as inhibitor of NF-κB activation in various cell types, such as intestinal epithelial cells, macrophages, and dendritic cells, influencing the production of proinflammatory cytokines, involved in the pathology of IBD [66]. The gene discussed is NFKB1; the disease is inflammatory bowel disease.