Platelets are activated in SCD particularly during vaso-occlusive episodes (VOE).8 Increased platelet activation likely plays a catalytic role in vaso-occlusion and vasculopathy in SCD 9,10 by increasing the adhesion of sickle RBCs to the endothelium11 via secretion of fibrinogen, von Willebrand Factor12 and Thrombospondin-1 (TSP1)13 and promoting further intimal damage.14 The gene discussed is THBS1; the disease is vascular disorder.