The defective Fas gene-mediated decreased functionality of regulatory T cells, accumulation of Th1 biased lymphocytes, and accumulation of anti-nucleic acid antibody-producing B lymphocytes drive an aggressive autoimmune phenotype relevant to many human autoimmune diseases including lupus, Sjogren’s syndrome, arthritis, and autoimmune lymphoproliferative syndrome (ALPS)32–35. This evidence concerns the gene FAS and systemic lupus erythematosus.