TNF is functionally central to RA pathophysiology and is involved in leukocyte activation, adhesion, and migration, in endothelial-cell adhesion molecule expression, and in stromal-cell, chondrocyte, and osteoclast activation (McInnes et al., 2016); IL-1 plays a role in destruction of bone at inflammatory joint sites, such as in RA, via activation, differentiation, and survival of osteoclasts (Kim et al., 2009), and it also mediates secretion of cytokines from synovial fibroblasts and monocytes and induces endothelial-cell adhesion molecule expression (McInnes and Schett, 2007). The gene discussed is IL1B; the disease is rheumatoid arthritis.