The release of inflammatory mediators by innate immune cells upon pathogen recognition, such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1, and their effect on endothelial cells, resulting in the activation of coagulation, vasodilation, endothelial leakage, rolling and extravasation of neutrophils and inflammatory mediators to the extravascular space, underscores the pathophysiology of organ dysfunctions and hypotension during sepsis (16). The gene discussed is IL6; the disease is Sepsis.