There are two ways for the contribution of the members of the TNF superfamily to IBD pathogenesis: (i) altering the intestinal epithelium integrity and inducing apoptosis in enterocytes (FasL, TNF, TWEAK, and TRAIL), and/or (ii) increasing the pro‐inflammatory activity of mucosa that infiltrate mononuclear cells (TL1A, TNF, TWEAK, LIGHT, and potentially FasL) and changing the activity of regulatory T cells and regulatory macrophages [56]. The gene discussed is FASLG; the disease is inflammatory bowel disease.