For example, Mackay et al. found that even though MZBs and B1a B cells induce the production of proinflammatory autoantibodies in BAFF-transgenic (BAFF-Tg) mice that develop an SLE-like phenotype, the depletion of B1a B cells or MZBs does not protect BAFF-Tg mice against disease [11]. This evidence concerns the gene TNFSF13B and systemic lupus erythematosus.