One such theory is that sublethal hypoxia upregulates several pro‐survival proteins, such as HIF1, Hsp, BDNF, and Bcl‐2, which then promote neuronal survival after cerebral ischemia or hypoxia.42, 43 However, neuronal survival in itself is not sufficient to protect the immature brain against H/I injury, as white matter injury is considered to be the leading cause of lifelong neurological deficits in survivors after H/I injury.13 This evidence concerns the gene BCL2 and Cerebral ischemia.