Furthermore, during maximal activation of coagulation, the endogenous fibrinolysis diminishes substantially in sepsis; when plasminogen activator (i.e., tissue plasminogen activator (t-PA)) and urokinase-type plasminogen activator (u-PA) are released from vascular endothelial cell storage sites, plasminogen activator stimulation and sub-quantitative plasmin production increase, whereas a continued increase in plasminogen activator inhibitor-1 (PAI-1) makes this effect disappear [62]. The gene discussed is PLAT; the disease is Sepsis.