New mechanistic work links ferroptosis, an iron-dependent form of cell death, to sepsis pathogenesis and organ dysfunction. The study maps lipid peroxidation and iron-handling pathways activated during severe infection, positioning ferroptosis as a modifiable node in the septic cascade. Complementing this pathophysiology, Hu and colleagues found baseline serum IgG concentrations stratify sepsis prognosis and identify patients who derive benefit from adjunctive therapies. Together the papers pair a mechanistic target (ferroptosis) with a clinically measurable biomarker (IgG) that could refine trial enrollment and therapeutic selection in critical care.