Proinflammatory cytokines TNF-α, IL-1β and IFN-γ, all of which have been implicated in SLE pathogenesis (80–82), suppress the expression of tight junction proteins, alter the arrangement of tight junctions, and modulate the actin cytoskeleton in intestinal epithelial cells, resulting in a compromised gut barrier (83, 84). The gene discussed is IFNG; the disease is systemic lupus erythematosus.