Abstract
The pathophysiology of sickle cell disease (SCD) is centered on the polymerization property of the desoxy-hemoglobin (Hb) S, but genetic factors can act as modulators of its clinical complications. Some of the genetic modulators are well known, as the presence of the alpha thalassemia and fetal hemoglobin (HbF) levels. Moreover, several othergenetic polymorphisms have been investigated, s…