The SESN2-dependent induction of AMPK activity and blunting of mTORC1 seem to bear substantial potential relevance to attenuate cell damage in conditions associated with acute ischemia, such as hypoxic-ischemic encephalopathy (HIE, caused by decreased oxygen and cerebral blood flow to the brain) or cardiomyocyte ischemia [74]. Here, SESN2 is linked to perinatal asphyxia.