Further, inhibition of PHD1 may improve oxygen radical detoxification and accordingly reduced detection of lipoxygenation through shunting glucose into the pentose phosphate pathway, as recently demonstrated in PHD1−/− neurons and in a model of cerebral ischemia in vivo.52 Further studies should reveal whether such reprogramming of the glucose metabolism is also involved in the protective effects of AQ and other PHD inhibitors in paradigms of oxidative cell death and at the level of mitochondria. Here, EGLN2 is linked to brain ischemia.