This supports the idea of a non-classical activation phenotype, rather than the rise of an immature neutrophil subset in the blood such as also has been described in sepsis patients.[48] Recently, also a circulating CD49dbright pro-angiogenic neutrophil phenotype has been described in mice in response to hypoxia-induced VEGF-A signaling.[33] It is possible that the neutrophils present at day 5–8 after cycling upregulate their CD49d because they are exposed to both DAMPs originating from limited reperfusion as well as hypoxia signals. The gene discussed is VEGFA; the disease is Sepsis.