To examine what MHC molecule is required for this autoimmune disease, we adoptively transferred whole Btla−/− SP thymocytes to KbDb−/− Rag−/− or CiiTA−/− Rag−/− mice that lacked both Rag and MHC class I genes or lacked both Rag and MHC class II protein expression [71], respectively. The gene discussed is BTLA; the disease is autoimmune disease.