There is ample evidence that the monoclonal antibody belimumab, which targets BAFF, can at least partially restore the impaired B-cell homeostasis in SLE by reducing B-cell activation and inhibiting the differentiation of autoreactive antibody-secreting cells through reduced binding of BAFF to its receptors BAFF receptor, TACI and BCMA [41,42,51]. This evidence concerns the gene TNFRSF13B and systemic lupus erythematosus.