Finally, variants that decrease the expression of alpha globin subunits (HBA1 and HBA2—alpha thalassemia)12,13 or allow for the persistent expression of gamma globin subunits into adulthood (HBG1 and HBG2 – persistence of fetal hemoglobin)14 can greatly mitigate the risk of death due to HbS homozygosity. This evidence concerns the gene HBG2 and alpha thalassemia spectrum.