For instance, in models of Mycobacterium tuberculosis infection and Staphylococcus aureus pneumonia, ACOD1 primarily exerts its effects through neutrophils,[64, 70] while in traumatic tendon injury models, neutrophils are identified as the primary ACOD1‐expressing cells regulating local inflammation.[71] These discrepancies may reflect variations in cellular activation patterns, inflammatory microenvironments, and metabolic states across different disease models. Here, ACOD1 is linked to staphylococcus aureus pneumonia.