Sickle cell disease (SCD) is a genetic disorder of the blood, causing anemia. It results from the polymerization of a mutated hemoglobin HbS, the oxygen-carrying protein found in red blood cells (RBCs), which causes the soft cells to deform into a rigid sickle shape under certain circumstances. Because the deformed cells induced by the polymerization will clog the blood capillaries, it induces an increase in blood pressure and ultimately degeneration of the various organs. Pharmacological treatments for sickle cell anemia include hydroxyurea, a molecule that promotes the synthesis of fetal hemoglobin (HbF) which leads to a mixture of hemoglobin HbFxHbS(1-x) in the blood, with HbF partially inhibiting polymerization of HbS. Gene therapy is also used for the treatment of this disease by stimulating the production of therapeutic hemoglobin (HbAt), or normal hemoglobin (HbA0). In collaboration with the Department of Genetic Diseases of the Red Blood Cell at Henri-Mondor hospital, we propose to study the effect of the addition of different types of hemoglobin on the polymerization process as well as the kinetics of oxygen capture at RBC level. This model study is directly linked to the treatments developed to cure this disease and aim to try to better understand them from a molecular point of view.