Our previous series of investigations revealed that AM pyroptosis and its inflammatory mediator, high mobility group box 1 (HMGB1), induced by cardiopulmonary bypass and sepsis led to the translocation of HMGB1 from the nucleus to the cytoplasm and ultimately to the extracellular fluid, thereby initiating and amplifying the inflammatory response and causing pulmonary damage [4,5]. This evidence concerns the gene HMGB1 and Sepsis.