The disproportionate host inflammatory response to pathogens during sepsis results in dysfunction and damage to the vascular endothelium, largely due to the effects of a cytokine storm, with inflammatory cytokines such as tumor necrosis factor a (TNFα), interleukins 1b and 6 (IL-1b and IL-6), and interferon-gamma (IFNg) being implicated [27]. This evidence concerns the gene TNF and Sepsis.