In fact, human IBD has been associated with an intense oxidative stress, excessive generation of ROS and RNS in the intestinal tissue which induces lipid peroxidation, protein modifications, DNA damage, and apoptosis, together with impairment of the enzymatic and non-enzymatic antioxidant mechanisms, including superoxide dismutase (SOD), and reduced glutathione (GSH) and catalase (CAT), which results in the colonic damage associated with intestinal inflammation [22,65]. This evidence concerns the gene CAT and inflammatory response.