Although RES's antiproliferative activity does not influence cell proliferation during CRC progression, it has been proven that RES can extensively target several mediators in CRC cells that are overexpressed (e.g., insulin growth factor1 (IGF-1)) and thereby suppress cell proliferation mediated by aberrant activation of Wnt β-catenin [103]. This evidence concerns the gene IGF1 and colorectal carcinoma.