Most pro-inflammatory cytokines (e.g. IFN-γ, TNF-α, and IL-1β) could reduce key TJ-associated proteins such as intracytoplasmic proteins (ZO-1, ZO-2) and transmembrane proteins (occluding and claudin), resulting in disruption of intestinal TJ barrier and the development of intestinal inflammation [50]. The gene discussed is TNF; the disease is inflammation.