Strikingly, neutrophil infiltration exhibited the strongest correlation with our biomarker panel (NAMPT: r = 0.68; SLC40A1: r = 0.62), suggesting S. aureus may manipulate granulocyte death pathways to optimize infection outcomes through either delayed apoptosis (intracellular persistence) or accelerated necroptosis (tissue damage). This evidence concerns the gene SLC40A1 and infection.