Therefore, our findings determined that MK2 participated in the overproduction of ROS by neutrophils in the pathogenesis of IBD and which might be based on the activation of Akt, p38 MAPK, and NADPH oxidase by MK2 in neutrophils and suggested that MK2 and ROS might be promising therapeutic targets for IBD. This evidence concerns the gene FMO5 and inflammatory bowel disease.