Because of the potential for functional redundancy between the Fas–FasL and perforin-dependent killing pathways, we also tested whether adoptive transfer of cells from diseased Rag−/− recipients of Prf1−/−PD-1−/− thymocytes to Faslpr × Rag−/− hosts would result in the development of autoimmunity. This evidence concerns the gene PRF1 and Autoimmunity.