Additionally, damage-associated molecular patterns (DAMPs), released from CDDP-injured PTECs, activate toll-like receptor (TLR)-4 on renal macrophages resulting in the production of inflammatory chemokines and cytokines which enable massive recruitment of circulating interferon gamma (IFN-γ) and interleukin (IL)-17-producing neutrophils and T cells in injured kidneys leading to the aggravation of AKI 2. This evidence concerns the gene IL17A and acute kidney injury.