CDX2 and neoplasm: 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.