Mice with autosomal recessive mutations in Fas (lymphoproliferative, lpr mice; lack Fas expression) and FasL (generalized lymphoproliferative disease, gld mice; lack FasL expression) genes develop a spontaneous autoimmune syndrome; produce autoantibodies and accumulate a large number of CD4−CD8− T cells in the secondary lymphoid tissues, leading to the progressive development of lymphadenopathy and splenomegaly (37, 38). This evidence concerns the gene FASLG and Splenomegaly.