This could explain why the same mutations on different β chromosomal backgrounds are associated with disease of different clinical severity.2,3 Increased levels of fetal hemoglobin (Hb F or a2 γ2) are of no consequence in healthy adults, but confer major clinical benefits in patients with sickle cell anemia (SCA) and β-thalassemia, diseases that represent major public health problems.4 Fetal hemoglobin (Hb F or a2 γ2) is predominant in red cells of the fetus and the newborn baby, and is largely replaced after birth by adult hemoglobin (α2β2). The gene discussed is GSTM1; the disease is sickle cell disease.