Taken together with observations from previous sections, these studies show that inactivation of Cdx2 along with Cdkn2a, Sfrp4, and Sox17, which are frequently inactivated in proximal colon cancers by epigenetic silencing, synergizes with Cdx2 loss to result in BRAFV600E-driven tumor in proximal, but not distal, colon-derived stem cells. Here, CDKN2A is linked to neoplasm.