Prevention of this apoptotic injury with inhibitors of the caspase enzymes [47], regarded as the final executioners in apoptosis or of over expression of anti-apoptotic proteins, has been shown to improve survival in animal models of less acute sepsis.[2,3] Critical mediators of this septic apoptotic injury include pro-apoptotic proteins such as BAX and activated caspase-3 [2,3]. The gene discussed is CASP3; the disease is Sepsis.