The mechanisms underlying this condition include (1) acceleration of tissue-type plasminogen activator (t-PA) release from endothelial Weibel–Palade bodies due to hypoxia [33–35] or from organ storage pools after destruction [35–38]; (2) plasminogen-to-plasmin conversion acceleration via the expression of urokinase-type plasminogen activator (u-PA) receptor [38–41]; and (3) plasminogen-to-plasmin conversion acceleration via annexin A2 and S100A10 heterotetramer expression on tumor cells [42–44] or endothelial cells due to thrombin, hypoxia, and hyperthermia [45–47]. This evidence concerns the gene PLG and neoplasm.