Once ferroptosis is initiated, the ferroptotic cells can release either excessive intracellular iron to facilitate bacterial overgrowth and aggravate the infection [14, 17] or DAMPs such as high mobility group box 1 (HMGB1) and lipid peroxides such as 4-hydroxynonenal (4-HNE) to activate inflammatory signaling pathways, intensify inflammation, and cause tissue and organ injury, thereby exacerbating the pathological progression of sepsis [18, 19]. This evidence concerns the gene HMGB1 and Sepsis.