Our results demonstrating that the activation of the IFNγ−mediated signaling pathway in patients with active sJIA without MAS and in patients with sHLH/MAS in remission is comparable to that observed in patients with other rheumatologic diseases provide evidence of a normal response of monocytes to IFNγ in these conditions. The gene discussed is IFNG; the disease is systemic-onset juvenile idiopathic arthritis.