The involvement of monocytes in the pathogenesis of SLE is well documented.91 Studies have revealed that monocytes excessively produce B-lymphocyte stimulator (BLyS), which promotes the survival and proliferation of B cells.92 In murine models, the inhibition of monocyte activation, differentiation, and migration has resulted in therapeutic effects.93 These findings suggest that targeting monocytes could be an alternative treatment strategy. Here, TNFSF13B is linked to systemic lupus erythematosus.