However, unlike the conditional Kim1 overexpression studies mentioned above (30), our data show that this increase in renal macrophages is associated with suppression of inflammatory cell activation in uninjured and injured PTEC DN RAR mouse kidneys after IRI-AKI, perhaps explaining why renal macrophage recruitment by Kim1 upregulation in PTEC DN RAR mice does not promote renal injury. This evidence concerns the gene HAVCR1 and acute kidney injury.