In these cases, mAbs are used to bind and thereby block, e.g., pro-inflammatory cytokines (e.g., TNF-α for the treatment of RA), disease-dependent pathological mediators (e.g., vascular endothelial growth factor (VEGF) in pathological angiogenesis), immuno-oncology (e.g., CTLA-4 inhibition to prevent downregulation of immune responses against cancer cells), or autoimmunity-related molecules (e.g., B lymphocyte stimulator (BLyS) for the treatment of patients with systemic lupus erythematosus (SLE)). The gene discussed is TNFSF13B; the disease is rheumatoid arthritis.