The kidney’s high oxygen demand for blood filtration renders it exquisitely sensitive to redox imbalance—an aberration common to both CKD and acute kidney injury (AKI) that, when coupled with iron dysregulation, unleashes ferroptosis: a non-apoptotic, iron-dependent form of regulated cell death driven by iron accumulation, lipid peroxidation, and antioxidant defense impairment (e.g., GPX4/SLC7A11 dysfunction), cascades to which the redox-sensitive kidney is uniquely predisposed. The gene discussed is GPX4; the disease is chronic kidney disease.