Due to persistent overactivation of the JAK/STAT signaling pathway, a large number of proinflammatory factors, such as interleukin (IL)-1, IL-6, IL-8, and IL-10, are produced at such high levels that patients with JIA are in a state of extreme inflammation, an important factor in JIA pathogenesis [4,5]. Tobias Schmidt et al. reported that in patients with JIA, once IL-6 binds to a receptor such as IL-6R or gp130 complex on the target cell membrane, its receptor dimerizes, resulting in autophosphorylation of JAK and activation of STAT3 into a dimer. This evidence concerns the gene SOAT1 and juvenile idiopathic arthritis.