Further evidence for the contribution of IL-1 in AOSD pathophysiology came from the pioneering work by Pascual et al. reporting that incubated peripheral blood mononuclear cells (PBMCs) with serum from patients with systemic form of juvenile idiopathic arthritis (SJIA), led to increased expression of innate immunity genes and release of large amounts of IL-1β [27]. The gene discussed is IL1B; the disease is juvenile idiopathic arthritis.