Given that each one of these cytokines plays an essential role in disease development and/or pathogenesis in mouse models of these autoimmune diseases [35], [80]–[88] and that elevated plasma levels of IL-6, TNFα, IL-17A and IL-21 are detected in patients with SLE [89]–[91], systemic sclerosis [90], [92], [93], rheumatoid arthritis [90], [94]–[96], Sjögren's syndrome [97]–[99], and Kawasaki disease [100]–[102], we propose that dysregulation of a proinflammatory cytokine network is the common mechanism by which BLK risk alleles promote autoimmune disease development. The gene discussed is BLK; the disease is rheumatoid arthritis.