Studies in several mouse models with alterations of components of the UPR specifically in intestinal goblet cells, or displaying an exacerbated ER response linked to a mutation in the Muc2 gene resulting in the accumulation of miss-folded protein, have underlined the complex interplay between goblet cells and the Muc2 mucin they secrete, and the ER-response in determining increased susceptibility to colitis [37–40]. Here, MUC5AC is linked to colitis.