HBA2 and Alpha-thalassemia: Rocha et al. and Ndour et al. have investigated the role of genetic variants within the beta S-haplotypes, Senegal haplotype (Xmn1-rs7412844), alpha-thalassemia (3.7kb or 4.2 kb HBA1/HBA2 deletion), NPRL3-rs11248850, and BCL11A-rs4671393 in modulating hyposthenuria and acidification deficit in SCD patients, but could not reveal a role for either of these variants, in adults and in patients of all ages, respectively [24,41].