Mice (Watanabe-Fukunaga et al., 1992) or humans (ALPS, autoimmune lymphoproliferation syndrome patients) (Rieux-Laucat et al., 1995) defective for Fas (Faslpr/lpr mice) or its ligand, FasL (Faslgld/gld mice), develop progressive lymphadenopathy and splenomegaly resulting from accumulation of excess mature T and B cells as well as “unusual” αβTCR+CD4−CD8−B220+ T cells. This evidence concerns the gene FAS and Splenomegaly.