Our human serrated CRC data highlight additional gene defects that may cooperate with Cdx2 inactivation and BRAFV600E expression in our mouse model, such as p16Ink4a and/or Trp53 mutations, and restricted gene targeting to the terminal ileum, cecum and colon as permitted with the CDX2-CreERT2 transgene may be useful in future studies to determine how additional gene alterations collaborate with the CDX2 and BRAFV600E defects in tumor progression and metastasis. This evidence concerns the gene CDX2 and colorectal carcinoma.