Both mechanisms, secondary and primary, of DIC, such as high levels of urokinase-type plasminogen activator (u-PA), annexin-II, tissue-type plasminogen activator (tPA), reduced the levels of plasminogen and α2-antiplasmin, and were present in APL (acute promyelocytic leukemia). Here, ANXA2 is linked to acute promyelocytic leukemia.