A promising role in targeting ferroptosis in IR-AKI is also alluded to, since it is known that cytoplasmic high-mobility group box 1 (HMGB1), a damage-associated molecular pattern molecule, leads to an increased tubular ferroptosis during IR-AKI, and a HMGB1 nucleocytoplasmic translocation promotes renal inflammation and kidney injury after I/R insult. The gene discussed is HMGB1; the disease is inflammatory response.