These data of Th17 plasticity, partially solve the literature debate on the pathogenic or protective role of Th17 cells in immunomediated disorders (48, 49), supporting the hypothesis that, at least in JIA, the Th1 subset, both classic and non-classic, is directly involved in the active phase of the disease when the clinical manifestations are evident, and that the pure Th17 cells acquire a pathogenic feature when they start to produce IFN-γ shifting toward the Th17/Th1 and the non-classic Th1 phenotype (18, 20, 40). The gene discussed is IFNG; the disease is juvenile idiopathic arthritis.