However, calprotectin activation converges in multiple pathways whose activation enhances the production of proinflammatory cytokines, namely tumor necrosis factor-α (TNF-α), IL-6, IL-8, IL-12/23, and IL-18 (110), which are known to be physiopathologically- and clinically-relevant in RA (Figure 2). The gene discussed is TNF; the disease is rheumatoid arthritis.