Although we and others showed a crucial role for STAT1 in IFNγ signaling and autoimmunity [76], we found STAT4 to be dispensable in the formation of spontaneous GCs, T cell activation, complement deposition in the kidney, or the generation of T helper 1 cells in various autoimmune- and SLE-prone mice [89]. Here, IFNG is linked to systemic lupus erythematosus.