Over the last years, it has become evident that sJIA pathogenesis is driven by the mix of autoimmune and autoinflammatory features, especially driven by IL-1, IL-6, and IL-18, and because of different symptoms, innate system—driven pathogenesis and different treatment efficiency, it is frequently grouped as one of the autoinflammatory syndromes rather than a classical autoimmune disease [4,5,6]. The gene discussed is IL1B; the disease is systemic-onset juvenile idiopathic arthritis.