In particular, the role of NK cells in AKI can occur by distinct mechanisms, including (i) NK cell recruitment and activation mediated by CCR5 chemokines (directly) or OPN (indirectly) secreted by TECs; (ii) secretion of neutrophil-attracting chemokines induced in TECs through the CD137–CD137L axis; iii) NK cell-mediated killing of TECs through NKG2D–NKG2D-L interactions. The gene discussed is CCR5; the disease is acute kidney injury.