Significant genetic disease modifiers are a co-inheritance of α-thalassemia (the α-3.7 globin gene deletion) [2] and the presence of fetal-haemoglobin (HbF) inducing genotypes at the three major quantitative-trait loci (QTL) for HbF persistence [3–8]: XmnI-HBG2, BCL11A and HMIP. Co-inheritance of α-thalassemia is associated with reduced haemolytic events in sickle cell patients, due to decreased intracellular concentrations of the defective haemoglobin (HbS) and thus a decreased likelihood of HbS polymerisation. This evidence concerns the gene HBG2 and thalassemia.