These results were different with our previous study in another mouse model of intestinal cancer – Muc2/p21 mice [13], in which we found that selenium supplemented in the Western-style high risk diet was able to inhibit intestinal tumorigenesis and the selenium alone was likely to induce JNK1 phosphorylation and to inhibit β-catenin and Cox-2. Here, MUC2 is linked to intestinal cancer.