During inflammation, platelets interact with neutrophils via Toll‐like receptor 4 (TLR4), promoting both NETosis and thrombosis.[12, 13] Additionally, NETs activate endothelial cells (ECs), damage the vascular barrier, and enhance neutrophil transendothelial migration, further promoting the formation of NETs.[14, 15, 16] This process establishes NETs as key mediators of the hyperactivation of inflammation and coagulation in sepsis. This evidence concerns the gene TLR4 and Sepsis.