Although in our previous studies [8] on children with JIA, we showed increased proteolytic–oxidative activity stimulated by the influence of pro-inflammatory cytokines, including TNF-α, which promotes the degradation of PGs, little is known about the effect on these transformations of the antagonist of the mentioned factor, i.e., etanercept (ETA, a recombinant TNF receptor-Fc fusion protein) used in the therapy of JIA. This evidence concerns the gene TNF and juvenile idiopathic arthritis.