Initial studies in mice indicated that loss of BIM or overexpression of BCL2 leads to the production of antinuclear autoantibodies, resulting in autoimmune disease resembling Systemic Lupus Erythematosus (SLE).156,486 In humans, SLE is associated with high levels of T cell-dependent antinuclear autoantibodies and systemic inflammation. This evidence concerns the gene BCL2 and systemic lupus erythematosus.