Since induction of ER chaperone GRP78 represents a major survival arm of ER stress response, and indeed, overexpression of ER chaperone is protective for cardiac myocytes from ischemia and calcium overload injuries [26], these observations could be in good accordance with the general view that the UPR has a protective role during initial phase of ER stress, while proapoptotic pathways are activated upon continued ER stress [12], [13], [14]. This evidence concerns the gene HSPA5 and ischemia.