As for hepatocytes and macrophages, cytosolic HMGB1 is capable to prevent deleterious cell death from endotoxemia by mediating autophagy and mitophagy (Fig. 2).112 Stress stimuli that enhance ROS could promote nucleocytoplasmic shuttling of HMGB1, where it directly interacts with the autophagy protein beclin-1 by displacing Bcl-2, thus resulting in formation of autophagy initiation complexes and removal of hazardous oxidative stress stimulus (Fig. 2).113 The various redox states of intracellular HMGB1 have contributed to its important regulatory role for AIM inflammasome activation. The gene discussed is HMGB1; the disease is serum lipopolysaccharide activity.