This work showed that removing the ability of cells to respond to either CCR2 or CX3CR1 was sufficient to prevent IRI-associated increases in serum creatinine within 24 h, thus implicating monocyte-derived cells in AKI and supporting a previous observation that the lack of CCR2 signaling was able to reduce ischemic kidney injury (145). This evidence concerns the gene CX3CR1 and acute kidney injury.