Using both in vitro models (PBMCs, pDCs), ex vivo samples from SLE patients’ bone marrow and peripheral blood, and an in vivo pristane-induced SLE mouse model, we sought to elucidate whether CB could serve as a potential therapeutic strategy for SLE by modulating CXCR4-dependent pathways. The gene discussed is CXCR4; the disease is systemic lupus erythematosus.