An 81-year-old Caucasian male was referred to emergency department for fatigue associated with profound anemia. He had type-2 diabetes previously treated with metformin, ischemic cardiac insufficiency, and stage-3 chronic kidney disease (CKD, CKD-Epidemiology Collaboration [CKD-EPI] estimated glomerular filtration rate: 32 mL/minute/1.73 m2). There were no clinical signs of infectious or tumoral disease. Vitiligo was observed on both hands. First biological tests revealed normocytic non-regenerative anemia associated with hemolysis, thrombocytopenia, and elevated sideremia, ferritin, and transferrin saturation (TSAT) levels. Vitamin B12 was undetectable, whereas vitamin B9 and C-reactive protein levels were normal. He received one pack of red blood cells (RBC), then was admitted to internal medicine department. A peripheral blood smear showed hypersegmented neutrophils, and a bone-marrow smear showed hypercellularity and clear signs of dyserythropoiesis and blocked maturation of erythroid cells. Stomach endoscopy and biopsies showed chronic gastritis and fundic atrophy. Though metformin may have participated in this condition [], a diagnosis of megaloblastic anemia caused by pernicious anemia was preferred considering the profound anemia and vitiligo, even if blood antiparietal cells or anti-intrinsic-factor antibodies were not detected. After two other packs of RBC and five daily intramuscular vitamin B12 injections, he was discharged and continued oral vitamin B12 supplementation. Three-month (M3) biological control revealed that platelet count and hemoglobin, sideremia, and TSAT levels normalized. Ferritin returned to normal values at 7 months (361 µg/L). We tested our hypothesis by analyzing the samples at the time of diagnosis and at M3 after receiving informed consent of the patient. Serum hepcidin, ERFE, and GDF15 levels were assessed by ELISA (hepcidin-25: S-1337, Peninsula; ERFE: ERF-001, Intrinsic LifeSciences; GDF15: DGD150, R&D Systems). Serum erythropoietin (EPO) was measured by chemiluminescence (UniCel DxL, Beckman Coulter). ERFE and GDF15 levels were higher than those of age-matched healthy controls (HC) at diagnosis, dropping to HC levels at M3, supporting our hypothesis. The level of hepcidin was lower at the time of diagnosis than M3 but remained within reference levels, and its kinetics from diagnosis to M3 inversely correlated with those of EPO, ERFE, and GDF15.