In the early stage of sepsis, by interacting with platelet hemostatic receptors (e.g. GPIIb/IIIa, GPIb) and immune receptors (e.g. FcγRIIa, TLRs), pathogens induce platelet activation, aggregation, and consumption, trigger systemic thrombosis, and obstruct the microvascular system, leading to ischemic injury to peripheral tissues and even organ failure. This evidence concerns the gene ITGA2B and Sepsis.