During sepsis, activated caspase-1 interacts with molecular events which promotes mitochondrial dysfunction, such as ROS production of mitochondria, disturbance of membrane permeability, and fragmentation of mitochondrial network, then exacerbates apoptosis with pro-inflammatory response (65). Apoptotic events orchestrated by elevated intracellular oxidative stress was suggested for pathogenesis of sepsis- induced acute respiratory distress syndrome (66). This evidence concerns the gene CASP1 and Sepsis.