A20 loss in B cells promotes cell survival and the establishment of an inflammatory microenvironment. Constitutive NFkB signaling in B cells lacking A20 induces expression of prosurvival genes, such as Bcl_XL, and up-regulation of proinflammatory cytokines, such as IL-6, which, in turn, stimulate the growth of immune cells. In the presence of such inflammatory conditions, chronically stimulated autoreactive B cells and plasma cells produce auto-antibodies causing autoimmune disease.