In both patients with SLE and in SLE mouse models, CD40L is overexpressed by T cells and ectopically expressed in B cells15–17, and this excess CD40L expression appears to play a role in development of SLE, as treatment with antagonistic anti-CD40L antibody markedly reduces the severity of the disease in both humans and mice18. This evidence concerns the gene CD40LG and systemic lupus erythematosus.