Our results solidify the notion that necroptosis occurs following tGCI-induced hippocampal neuronal damage and add to the existent body of evidence suggesting that blocking necroptosis with hypoxic preconditioning can protect against neuronal injury during cerebral ischemia, and that MLKL may be a potential therapeutic target for the treatment of cerebral ischemia. This evidence concerns the gene MLKL and Cerebral ischemia.