Constitutive over-expression of BAFF in BAFF-Tg mice otherwise not autoimmune-prone leads to systemic lupus erythematosus (SLE)-like features [20]–[22], and treatment of SLE-prone mice with a BAFF antagonist ameliorates disease [22]–[24]. This evidence concerns the gene TNFSF13B and systemic lupus erythematosus.