Oxidative stress is reported to trigger the translocation of HMGB1 from the nucleus to the extracellular space [126, 127], and antioxidants are reported to be protective in the setting of experimental infection/sepsis and injury, including ischemia‒reperfusion, partly by attenuating HMGB1 release and systemic accumulation [128]. This evidence concerns the gene HMGB1 and infection.