Neutrophils play a critical role in the early phase of sepsis by phagocytosing and eliminating pathogens.[28] However, their excessive activation can lead to the release of reactive oxygen species, neutrophil extracellular traps, and proteases, which damage the endothelial barrier and trigger systemic inflammation.[29] In this study, elevated expression of SIGLEC5, PIM3, and NEDD4 was positively correlated with neutrophil infiltration, suggesting that these genes may facilitate neutrophil recruitment by regulating cytokines and chemokines. The gene discussed is SIGLEC5; the disease is Sepsis.