By comparison in colonic adenocarcinomas, elevated β-catenin levels caused by mutations in CTNNB1 or APC result in activation of the Wnt/β-catenin/LEF1 pathway through a LEF1 binding site in the cyclin D1 promotor, triggering cyclin D1 gene expression, and subsequently, uncontrolled progression of tumor cells into the cell cycle [8, 12]. Here, LEF1 is linked to neoplasm.