The generation of ROS per se seems likely to be a physiological event that contributes to the regulation of general metabolic health, such as mediating phagocyte killing of bacteria. Another physiological function is to modulate transcription of genes, such as nuclear factor-κB (NF-κB), a well-known redox-sensitive transcription factor. However, the elegantly designed host-defense mechanisms against ROS provided by antioxidant enzymes and GSH synthesis (Fig. 4) (rev. in 54,55) imply that ROS levels need to be finely regulated to keep good radicals from going bad and thereby avoid oxidative damage to cellular processes (56).