Primary hyperfibrinolysis in APL relies on tissue plasminogen activator (tPA), urokinase plasminogen activator (uPA), and annexin II, while secondary hyperfibrinolysis relies on systemic breakdown of clots and microvascular clotting/lysis typically seen in disseminated intravascular coagulopathy (22, 23). The gene discussed is PLAT; the disease is acute promyelocytic leukemia.