On the basis of the “dual pathway model”, Lim, C. L. 30 suggested that the endotoxemia pathway of heatstroke was mediated primarily by endotoxemia and systemic inflammatory response, ultimately leading to sepsis, which meant that excessive LPS leaked from gut activates TLR4 on monocytes in circulation to product pro-inflammatory cytokines 20. The gene discussed is TLR4; the disease is Sepsis.