BRAF and neoplasm: These molecular effects of Cdx2 loss resulted in acquisition of transient Wnt-independent growth in the proximal but not distal colon-derived organoids, which further specifically resulted in transformation of only the proximal colon stem cells by mutant BRAF. This dependency on Cdx2 for maintaining stem and differentiation programs and tumor development by BRAF specifically in proximal colon stem cells strongly suggests that the underlying transcriptional states and its regulation play central roles in defining differences in tumors along the colonic axis.