These mechanisms evidence the pathogenetic role of CD4+ Th cells in JIA pathophysiology and allow a better comprehension of the involvement of Th17 cells and their own ability to produce IFNγ, shifting toward the Th17/Th1 and the non-classic Th1 phenotype after appropriate cytokines’ stimulation (Figure 3) [27,32]. The gene discussed is CD4; the disease is juvenile idiopathic arthritis.