A wide variability in severity and clinical presentation is driven partially by additional genetic factors, such as the genotypic state at the site of mutation (homozygous: Hb SS; compound heterozygous: Hb SC, HbS beta thalassaemia) and by genetic disease modifiers at the beta-globin gene locus or elsewhere in the genome. The gene discussed is GSTM1; the disease is beta thalassemia.