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Martin K Safo*, Andrew N Fleischman and Osheiza Abdulmalik
hematologic disorder, affecting about 20 million people worldwide. The disease arises from a single-point mutation (βGlu6 → βVal6) in the β-globin gene of Hemoglobin (Hb), resulting in sickle Hb (HbS). The primary pathophysiology of SCD involves hypoxia-induced HbS polymerization to form insoluble fibers as a result of a unique interaction between βVal6 protrusion of HbS tetramers and a hydrophobic pocket on an adjacent HbS tetramers, causing sickling of red blood cell (RBCs).