These Th1 cells, which produce high levels of TNFα and IFNγ, are particularly implicated in the pathology of RA, SLE, and Crohn’s disease [55–58] where neutrophils are also shown to contribute to pathology, highlighting the interdependency and co-regulation of the innate and adaptive immune systems during cytokine-driven inflammation. The gene discussed is TNF; the disease is rheumatoid arthritis.