Our analysis indicates that our selection, comprising 18 HBB (“hemoglobin”) mutations, as well as 2 HFE (“hemochromatosis”) mutations, provides excellent coverage: all but one of the patients in our multi-ethnic cohort of 274 (predominantly) pediatric and adolescent Pakistani β-thalassemia patients in fact had at least 1 of the selected mutations (Table 1). This evidence concerns the gene HBB and hemochromatosis.