The results of treatment with AMG 108 instead appear to point to a limited role of IL-1 in human RA synovial inflammation - a notion supported by the profound effect seen with other IL-1 inhibitors in conditions other than RA, such as systemic-onset juvenile idiopathic arthritis, gout, neonatal-onset multisystem inflammatory disease, cryopyrin-associated periodic syndromes, and other autoinflammatory disorders [28,29]. This evidence concerns the gene IL1B and systemic-onset juvenile idiopathic arthritis.