During sepsis, lipopolysaccharide upregulates JAK-STAT/NF-κ B pathway expression and increases the release of inflammatory mediators (IL-6, TNF-α and IL-10) through Toll-like receptor interactions with innate immune cells during sepsis, leading to alveolar epithelial cell and vascular endothelial cell injury, which in turn causes diffuse acute lung injury [4, 25]. This evidence concerns the gene SOAT1 and Sepsis.