The accumulation of damage caused by reactive oxygen species (ROS) is held to be one of the underlying causes of age-related decline and has been shown to be involved in a number of pathological states. Inherent defense mechanisms have evolved to limit this damage by reducing the levels of ROS, which are produced mainly by the mitochondria in aerobic organisms. One such defense is superoxide dismutase 1 (SOD1). It is well established that oxidative stress results in increased transcription and translation of the SOD1 gene, but it is now known that an additional level of posttranslational control exists. A recent paper describes the presence of an inactive pool of SOD1 whose activation is wholly reliant on the presence of superoxide or oxygen and a specific copper-containing chaperone. This mechanism highlights the importance of rapid responses in the fight against oxidative stress.