DMH-colon cancer is primarily dependent on its biotransformation into more reactive intermediates, which takes place via two pathways: glutathione (GSH) conjugation and cytochrome P450 monooxygenases (CYPs)-dependent oxidation (phase I) (phase II) [20]; positive alterations in blood Ca19.9, CEA, and AFP levels were caused by the release of reactive oxygen species (ROS), which harm the colon and create instability in colon cell metabolism. This evidence concerns the gene CYP20A1 and colonic neoplasm.