Inhibiting the interaction of the ligand with its receptor in animal models or human studies provided support to the pathogenic signature of the CD154/CD40 axis in numerous diseases of inflammatory and/or autoimmune nature, including rheumatoid arthritis (RA) [39], multiple sclerosis [40], autoimmune thyroiditis [41], polymyositis, dermatomyositis [42], inflammatory bowel diseases [43], and SLE. The gene discussed is CD40; the disease is systemic lupus erythematosus.