Furthermore, as NF-κB is the final common pathway or rate-limiting step in the inflammatory cascade, if the therapy interferes with the NF-κB pathway (the upstream target) in the cascade of inflammation, it will block the expression of multiple proinflammatory genes simultaneously, which might be more effective than suppressing individual factors such as TNF-α, IL-1β, and IL-6 in the treatment of intestinal inflammation [1]. This evidence concerns the gene NFKB1 and inflammation.