Alveolar CXCL2 was able to induce extravasation of comparably more intravascular neutrophils in sham mice than in AKI mice (Supplemental Figure 8), indicating that neutrophil stiffness, which was more prominent in AKI neutrophils (Figure 4), at least partially contributed to the neutrophil intravascular retention phenotype. This evidence concerns the gene CXCL2 and acute kidney injury.