In the early immune response, the source of IL-6 is primarily from innate immune cells activated by toll-like receptor (TLR) binding of pathogen-associated molecular patterns (PAMPs) and by the secretion of IL-1α/β, TNF-α, IFN-γ, and/or granulocyte-macrophage colony stimulating factor (GM-CSF) by monocytes and macrophages.6 IL-6 usually enhances TLR-mediated cytokine and chemokine production; however, IL-1β, TNF-α, and IL-8 (CXCL8) production is suppressed by IL-6 when TLR4 binds its ligand, lipopolysaccharide (LPS), thus providing protection against endotoxemia.8 The gene discussed is IL6; the disease is serum lipopolysaccharide activity.