In sepsis, the core mechanism driving renal ferroptosis is the dysregulation of lipid peroxidation, whereby sepsis suppresses the renal amino acid–dependent antioxidant system—characterized by reduced GSH levels and impaired GPX4 activity—resulting in excessive lipid peroxide accumulation and ultimately triggering ferroptosis in renal tubular epithelial cells [6]. This evidence concerns the gene GPX4 and Sepsis.