REDD-1, also designated DNA-damage-inducible transcript 4, dig2 or RTP801, is thought to function in the regulation of reactive oxygen species (ROS). REDD-1 expression has also been linked to apoptosis, Ab toxicity and the pathogenesis of ischemic diseases. As an HIF-1-responsive gene, REDD-1 exhibits strong hypoxia-dependent upregulation in ischemic cells of neuronal origin. In response to stress due to DNA damage and glucocorticoid treatment, REDD-1 is upregulated at the transcriptional level. REDD-1 negatively regulates the mammalian target of Rapamycin (mTOR), a serine/threonine kinase often referred to as FRAP. It is crucial in the coupling of extra- and intracellular cues to FRAP regulation. The absence of REDD-1 is associated with the development of retinopathy, a major cause of blindness.