The pathogenesis of JIA is associated with aberrant activation of phagocytes (monocytes, macrophages, and neutrophils), suppression of Treg cells, hyperactivation of Th1 and Th17 cells, activation of NF-κB, and proinflammatory cytokines (IL-1, IL-6, IL-17, IL-18, IL-21, IL-22, IL-23, Interferon-γ [IFNγ] and TNF-α) (100–103). The gene discussed is NFKB1; the disease is juvenile idiopathic arthritis.