The activation of TLRs, as well as stimulation by NETs—primarily through the NF-κB signaling pathway—elicits proinflammatory and pro-thrombotic responses in endothelial cells, activating platelets and stimulating the deposition of fibrin, thereby contributing to the amplification of vascular inflammation, blood clot formation and the overall pathogenesis of sepsis (11, 12, 110). The gene discussed is NFKB1; the disease is Sepsis.