Complementary evidence further shows that Neu3 is responsible for desialylation and deficiency of intestinal alkaline phosphatase (IAP) during recurrent infection, whereas Neu3-null mice retain IAP and are protected from colitis [73], positioning NEU3 as a regulator of gut barrier integrity that is probably mechanistically linked to metabolic disease–associated GI inflammation. This evidence concerns the gene NEU3 and colitis.