Sickle cell anemia (SCA) is a genetic disorder characterized by a high inter-individual clinical variability partly related to the existence of various genetic modulators such as hemoglobin F (HbF) quantitative trait loci (QTL), alpha-thalassemia, and glucose-6-phosphate dehydrogenase (G6PD) deficiency [1]. This evidence concerns the gene G6PD and alpha thalassemia spectrum.