In this work we show that the appropriate responses to anemia and tissue hypoxia (using repeated phlebotomies as the "gold standard") are deranged at several levels in this model of CKD in young rats: renal HIF2 α is not increased (Fig 1b), circulating as well as bone marrow EPO (which reflects circulating EPO, since no EPO is synthesized in BM [5]) is not increased. This evidence concerns the gene EPO and chronic kidney disease.