During IBD, infiltrated monocytes and immature macrophages in inflamed mucosa stay responsive to TLRs, contributing to an upregulation of pro-inflammatory mediators (e.g., IL-1β, IL-6, IL-12, TNF-α, iNOS) and bolster respiratory burst activity, and downregulation of IL-10, leading to monocyte infiltration, tissue damage and function deterioration [11, 24, 28, 40, 45, 50, 133, 134]. The gene discussed is TNF; the disease is inflammatory bowel disease.