This group focused on the T cell-intrinsic role of excess IFNγ in autoimmunity development and showed that increased IFNγ signaling caused Bcl-6 overexpression in T cells, leading to an accumulation of Tfh cells, GC B cells, and autoantibodies and development of lupus nephritis in Roquinsan/san mice (Figure 2). The gene discussed is IFNG; the disease is Autoimmunity.