A separate study showed that, in a genetic model of CRC (i.e., genetically sensitized MSH2 and MLH1 -deficient mice), the gut microbiota stimulated polyp formation by providing butyrate that induced hyper-proliferation and transformation of colon epithelial cells, suggesting a role of butyrate-producing gut microbes in the etiology of CRC [72]. This evidence concerns the gene MLH1 and colorectal carcinoma.