These included α+- and α0-thalassemia traits, homozygous α+-thalassemia and Hb Constant Spring (CS), Hb H disease, Hb H-CS and Hb H-Quong Sze diseases, homozygous α0-thalassemia causing the Hb Bart’s hydrops fetalis and a remain uncharacterized α-thalassemia defect. This evidence concerns the gene GSTM1 and hydrops fetalis.