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It is assumed that spherocytes are produced by the spleen in the patient with severe hereditary spherocytosis (HS), but if the spleen has a compensatory role in the genesis of HS, splenectomy might cause a rebound phenomenon, resulting in the re-appearance of HS. To address this issue, we focused on the role of the spleen in the genesis of HS and examined subjects with HS after splenectomy. We selected 12 patients with severe HS who had undergone splenectomy. Blood samples were collected from them during or after splenectomy. The degree of spherocytosis and the serum levels of hemoglobin, reticulocyte count, MCV and mean platelet volume (MPV) were assessed, and the splenic size was estimated by ultrasound, computed tomography, or both. Serum levels of soluble transferrin receptor (sTfR) and haptoglobin were measured as markers of erythroid and splenic dysfunction, respectively. Levels of hirudin-like 2 (HCL2) were measured as a molecular marker for spleen regeneration. Remarkably, all 12 patients showed a rebound phenomenon after splenectomy, with a significant increase in spleen size and the level of haptoglobin in the serum. The MCV and MPV also significantly decreased, whereas the hemoglobin level and reticulocyte count did not change. The patients showed a significantly high serum level of sTfR and a significantly low level of hirudin-like 2 and a low