We anticipated that the lesions in the IL-18-deficient mice would be attenuated, since we speculated that IL-18 might accelerate skin inflammation through a mechanism phenotypically similar to that involved in the effect of anti-IL-18 therapy in autoinflammatory IL-18-driven diseases, such as familial Mediterranean fever and systemic juvenile idiopathic arthritis [27–29]. The gene discussed is IL18; the disease is systemic-onset juvenile idiopathic arthritis.