Since it was not clear how colon GCs survive by producing highly efficient MUC2, which induces ER stress through misfolded MUC2 proteins, a subsequent study on cultured colorectal adenocarcinoma cells (HT29) showed that high MUC2 biosynthesis actually dysregulated the autophagy processes controlled by IL-22 to maintain the intestinal barrier of innate host defense [150]. Here, MUC2 is linked to colorectal adenocarcinoma.