It should be emphasized that Stanniocalcin-2 upregulation unrelated to IGF signaling is also possible; this upregulation might be also activated in response to oxidative stress and hypoxia after coronary artery occlusion in a similar way to what had been demonstrated in the animal model after cerebral artery occlusion [28] or in the setting of hypoxic tumor microenvironment [29]. This evidence concerns the gene STC2 and neoplasm.