Experimental models (lipopolysaccharide (LPS), cecal ligation and puncture (CLP) and pathogen-specific models) reveal GPX4 downregulation, increased lipid peroxidation and iron redistribution in affected organs; pharmacologic or genetic inhibition of ferroptosis (e.g., Fer-1, liproxstatin-1, GPX4 preservation) reduces tissue damage and improves outcomes in multiple preclinical sepsis models [216]. Here, GPX4 is linked to Sepsis.