Together, small molecules that degrade both β-catenin and RAS via the transcriptional repression of EGFR can be a potential therapy for the treatment of CRC patients with aberrantly activated Wnt/β-catenin and EGFR-RAS pathways attributed to the increase in β-catenin, EGFR, and RAS as well as to their activation by pathologically important APC, KRAS, and EGFR mutations. This evidence concerns the gene EGFR and colorectal carcinoma.