The polymerization of hemoglobin S (Hb S) within the cell is the central event that occurs in the pathophysiology of SCA; however, there is increasing evidence that nitric oxide (NO) sequestration by cell-free Hb and impaired bioavailability of NO during intravascular hemolysis also play important roles in SCA pathophysiology (1,2). Here, GSTM1 is linked to autosomal dominant cerebellar ataxia.