The initial innate immune response in sepsis is triggered by exposure to damage-associated molecular patterns (DAMPs), leading to the transcription and release of type I interferon (IFN-1) and pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), IL-6, and IL-18 [15-16]. The gene discussed is TNF; the disease is Sepsis.