Because cytokines produced by B cells following BCR and/or Toll-like receptor (TLR) stimulation have been described as playing an important role in autoimmune diseases [8], and because epratuzumab is able to partially inhibit BCR responses [6], in the present study we analyzed whether the antibody also has the capacity to modulate in vitro the cytokine production (IL-6, tumor necrosis factor [TNF]-α and IL-10) by B cells from patients with SLE compared with healthy donors (HD) upon BCR cross-linking alone or in combination with TLR9 stimulation. The gene discussed is TNF; the disease is systemic lupus erythematosus.