More recently, an increased membrane binding of both monomers and dimers of Prdx2 was found to be significantly higher in erythrocytes of SAD mice, a transgenic mouse model of sickle cell disease, than in wild-type mouse red cells under normoxia, suggesting protection against membrane oxidative damage characterizing sickle red cells by the chaperone action of Prdx2. This evidence concerns the gene PRDX2 and sickle cell disease.