The answer comes from a publication dissecting multi-step CRC development after oncogenic BRAF knock-in in the mouse [6]: activation of BRAF resulted in generalized intestinal hyperplasia with a reduced stem cell pool, and only progressive foci displayed activating mutations in the Wnt/β-Catenin pathway, nuclear β-Catenin and increased gene expression of Wnt targets and stem cell markers. This evidence concerns the gene BRAF and colorectal carcinoma.