In LPS‐stimulated bone marrow‐derived macrophages, UA inhibits TLR4 expression and IκB phosphorylation blocking NFκB signaling, thereby reducing the transcription of pro‐inflammatory genes.[75] However, butyrate enhances TLR4‐mediated NFκB signaling in colon cancer cells potentiating the antitumor innate immunity.[76] Although UA and butyrate display converse functions in NFκB signaling, they both prevent colon cancer progression by acting on different cell types. The gene discussed is NFKB1; the disease is colonic neoplasm.