RTP801 was initially identified as a gene induced by DNA damage, and later found to also be regulated by other cellular stresses such as hypoxia and glucocorticoid treatment.  Recently, RTP801 has been shown to act as a mediator of tuberous sclerosis complex (TSC)-dependent regulation of the mammalian Target of Rapamycin (mTOR), an evolutionarily conserved serine/threonine kinase that regulates cell growth and cell cycle.   In response to energy stress, RTP801 inhibits mTOR function, resulting in dephosphorylation of downstream targets such as ribosomal protein S6 kinase 1 and 4EBP1 and decreasing cell growth.  Disregulation of RTP801 may thus contribute to human tumorigenesis.