This feature reflects the complex pathophysiology of SCA which can be affected by a number of modifying factors including haplotype of β-globin gene cluster [4], coinheritance of polymorphisms associated with clinical aspects [5,6] and treatment response [7], hemoglobin fetal (Hb F) levels [8], chronic inflammation and oxidative states [9,10] as well as gender [4]. The gene discussed is GSTM1; the disease is autosomal dominant cerebellar ataxia.