However, Mgat5−/− mice have been reported to be more susceptible to inflammatory bowel disease [29], and MGAT5 variants in patients have been implicated in ulcerative colitis [30]; thus, in combination with intestinal inflammation described in Npc1−/− mice [31], the combined deficiencies may have exacerbated this problem, resulting in a runted state of the Mgat5−/−:Npc1−/− mice. This evidence concerns the gene NPC1 and ulcerative colitis.