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. This evidence concerns the gene TLR4 and colonic neoplasm.