Activation of NF‐κB signaling in innate immune cells such as monocyte and macrophage leads to increased expression of various pro‐inflammatory mediators including cytokines (such as TNFs, IL‐6, etc.), chemokines (such as monocyte chemotactic protein‐1, MCP‐1), adhesion molecules (such as E‐selectin), and enzymes (such as cyclooxygenase‐2), which remarkably prompts the onset of SIRS.17 The gene discussed is IL6; the disease is systemic inflammatory response syndrome.