The finding that the upregulation of adhesive molecules, such as P-Selectin (58, 59), or the loss of thrombomodulin (59, 68), may drive the complement attack on the endothelium, prompted us to investigate whether S1 protein-induced endothelial dysfunction could modulate complement activation and deposition on the microvascular endothelium. The gene discussed is THBD; the disease is endothelial dysfunction.