Normal colonic epithelial cells and adenoma cells are continuously exposed to high concentrations of highly hydrophobic bile acids and resist apoptosis induced by hydrophilic or low concentrations of hydrophobic bile acids, such as UDCA, and overactivate the EGFR/MAPK signaling pathway, resulting in irreparable oxidative DNA damage of intestinal epithelial cells and destroying the intestinal barrier to induce CRC (87). Here, EGFR is linked to colorectal carcinoma.