These findings suggest that TNFα might be a key player forming a positive feedback circuit in maintaining the pathology of corticosteroid-refractory systemic flare of AOSD in this patient and higher-dose etanercept might be required to suppress the disease activity of refractory AOSD patients with partial response to etanercept at its approved dose for the treatment of rheumatoid arthritis. The gene discussed is TNF; the disease is adult-onset Still disease.