Studies have noted an elevation in circulating IgG anti-neutrophil antibodies leading to complement activation [17] and an increase in TNF-related apoptosis inducing ligand (TRAIL) level [18, 19], as well as evidence for T cell- and monocyte-mediated suppression of granulocytopoiesis in the bone marrow of SLE patients [20]. This evidence concerns the gene TNFSF10 and systemic lupus erythematosus.