Endothelial cell expression of cathepsins and increased cathepsin-mediated elastase activity are upregulated during atherosclerotic development and induced by inflammation and altered hemodynamics [9, 12, 13, 26, 27], which are both present in sickle cell disease [26], leading to our hypothesis that elevated TNFα and increased circulating mononuclear cells would stimulate increased endothelial cell cathepsin activity. The gene discussed is CTSS; the disease is sickle cell disease.