In a murine model of septic shock, AC-YVAD-CMK, a specific caspase-1 inhibitor, demonstrated a protective influence on vital organs such as the liver, brain, and lungs [239-241] by reducing NLRP1 inflammasome expression and inhibiting inflammasome pathway-mediated sepsis in renal tubular epithelial cells, attenuating NLRP1 inflammasome-triggered secretion of the proinflammatory cytokines IL-1β and IL-18, sepsis-induced acute kidney injury, and histological damage to renal tissue, and inhibiting neutrophil and macrophage aggregation in renal tissue [242]. The gene discussed is NLRP1; the disease is acute kidney injury.