Clinical trials have proved the central role of TNF in the pathogenesis of RA (Smolen and Emery, 2011), and preclinical studies have extended our understanding of how TNF drives the classic pro-inflammatory response of FLSs by activating the NF-κB and mitogen-activated protein kinase (MAPK) pathway (Bartok and Firestein, 2010, Lee et al., 2013a). The gene discussed is NFKB1; the disease is rheumatoid arthritis.