ERCC1 and polycythemia: At present, we do not know the mechanistic basis for the exuberant polycythemia in response to hypoxia in Ercc1 Δ/- mice, but it is noteworthy, because if the therapeutic mechanism of hypoxia is dependent on achieving decreased brain oxygen tension, as it is for mouse models of mitochondrial neurological disease [28], a compensatory increase in hematocrit that augments brain oxygen delivery might blunt the beneficial effect of hypoxia over time.