Although UC can be triggered by bacteria, viruses, and other environmental factors, the inflammatory process of the intestinal mucosa is ultimately induced by soluble inflammatory mediators.30 The inflammatory mediators such as IL-1beta and TNF-α play leading roles in the development of UC.31 Therefore, the effective reduction of inflammatory mediators in the serum and colon tissues is a reasonable modality for UC treatment.32,33 Additionally, the anti-inflammatory effects of SOCS1 in immune disease have been uncovered. This evidence concerns the gene SOCS1 and immune system disorder.