We have hypothesized that PTCs under hypoxic/hyperglycemic/inflammatory conditions contribute to AKI through a pro-inflammatory response that involves an increase in their expression of leukocyte adhesion molecules and inflammatory chemokines in a DPP-4-, COX-2-, EP receptor- and PGT-dependent manner (which, in turn, would facilitate acute inflammatory responses involving neutrophils and monocytes/macrophages [4]). This evidence concerns the gene SLCO2A1 and acute kidney injury.