Because it has been shown that the predominant mechanisms of tumor progression differ between mucinous carcinoma cells and colorectal adenocarcinoma cells [66], these differences in cell types from which tumors and pre-neoplastic lesions can develop, may explain why Selenof-KO mice appear to be protected initially against ACF formation, but not AOM/DSS-induced tumorigenesis. Here, SELENOF is linked to neoplasm.