Although there are now ~128 different molecular defects known to cause α thalassaemia and an ever increasing number of potential interactions, the clinical phenotypes (broadly classified as α thalassaemia trait, HbH disease and Hb Bart's hydrops foetalis) resulting from the interactions between these various molecular defects can be simply summarised as in Table 3. This evidence concerns the gene GSTM1 and hemoglobin H disease.