Sickle cell anemia is one of the world’s most common monogenic disorders.1 It is caused by a mutation in the beta-globin gene’s sixth codon, which leads to the synthesis of an abnormal hemoglobin called hemoglobin S (HbS).2 The mutation can be heterozygous (Hb AS), homozygous (Hb SS), or combined with other hemoglobin defects, such as the -globin gene (Hb SThal), to cause sickle cell trait (SCT) and beta-thalassemia (T). This evidence concerns the gene GSTM1 and beta thalassemia.