HLH is a hyperinflammatory phenotype rather than a single disease, wherein heterogeneous triggers, including infections, rheumatologic conditions, malignancies, and genetic HLH, culminate in a final common pathway of overactive T cells and macrophages that secrete enormous amounts of proinflammatory cytokines, such as interferon (IFN)-gamma, interleukin (IL)-1-beta, IL-2, IL-6, IL-10, IL-18, and tumor necrosis factor (TNF). This evidence concerns the gene TNF and hemophagocytic syndrome.