First, the identification of rTEM PMNs relied on surface phenotype markers, specifically high ICAM1 and CXCR4 expression and low CXCR1 expression, which is consistent with the findings of most previous studies.[10, 37] Although an advanced in vivo cell labeling technique has recently been reported,[9, 31] providing direct evidence of PMN rTEM occurrence and tracking rTEM PMNs from a local site to the lungs, this method is not applicable to systemic inflammation models such as sepsis. Here, CXCR4 is linked to Sepsis.