Targeted deletion of regulatory molecules associated with SLE susceptibility in humans, including Shp1, A20, Blimp-1, Lyn, or Eat-2, specifically in CD11c+ cells resulted in increased DC activity and development of inflammatory and autoimmune phenotypes characterized by the production of autoreactive antibodies and several manifestations of SLE, including severe glomerulonephritis [128–132]. This evidence concerns the gene PRDM1 and systemic lupus erythematosus.