The most prevalent combinations were SCT plus heterozygous α+ AT without G6PD deficiency (HbAS, heterozygous α+ AT, G6PD(B)) in 41/431 (10.2%), followed by heterozygous α+ AT plus heterozygous G6PD deficiency without SCT (HbAA, heterozygous α+ AT, G6PD(A)) in 18/431 (4.2%) and SCT plus homozygous α+ AT without G6PD deficiency (HbAS, homozygous α+ AT, G6PD(B)) in 11/431 (2.6%) (Table 2). This evidence concerns the gene G6PD and G6PD deficiency.