As TNF-α is a key mediator in the pathological mechanisms of a large number of neurological disorders including ischemia, AD, PD, MS, and ALS [3] and also in peripheral autoimmune disorders including rheumatoid and juvenile arthritis, ankylosing spondylitis, and Crohn's disease, targeting TNF-α action seems to be an attractive disease-modifying strategy. This evidence concerns the gene TNF and juvenile idiopathic arthritis.