For example, a recent study in antiphospholipid syndrome demonstrated that heparanase activity promotes tissue factor overexpression in endothelial cells and platelets through IL-1 receptor-associated kinase (IRAK1) and NF-κB signaling, thereby linking IL-1β with extracellular matrix–remodeling enzymes and vascular immune activation [33]. This evidence concerns the gene NFKB1 and antiphospholipid syndrome.