Hence, we postulate that the presence of CD36 on the surface of immature sickle reticulocytes may contribute to the pathophysiology seen in SCA-associated vasculopathy, based on the associations observed between the higher ARC in patients with MRA-documented cerebrovasculopathy prior to initiating CTT which was unchanged after a year of CTT. The gene discussed is CD36; the disease is autosomal dominant cerebellar ataxia.