These include (I) hemoglobinopathies, such as SCD, and thalassemia, which are well-described human genetic defects; (II) defects of cytoskeletal proteins, mainly described in transgenic mice; and (III) redox dysregulation related to genetic defects leading to increased production of oxidants and/or decreased antioxidant capacity, which ultimately lead to hemolytic anemia. This evidence concerns the gene DNM2 and thalassemia.