Sepsis activates neutrophil extracellular traps through pathogen-associated molecular patterns, providing a scaffold for von Willebrand factor and tissue factor, thereby promoting microvascular thrombosis.[10] Concurrent with the thrombotic risk is the inherent bleeding tendency of ET.This presents substantial challenges in thrombo-hemorrhagic management when “ET + STEMI + Sepsis” coexist as a triple pathological burden. The gene discussed is F3; the disease is Sepsis.