GSDMD and Sepsis: In the LPS‐induced sepsis model, caspase‐11 and GSDMD knockout mice (GSDMD−/− mice) showed significantly improved survival rates.[11] Mechanistically, activation of the caspase‐11/GSDMD pathway controls the neutrophil extracellular trap (NET) release from neutrophils during sepsis.[12] Inhibition of GSDMD with disulfiram or genetic deletion can eliminate excessive NET formation, thereby reducing organ dysfunction and mortality in sepsis.