Therefore, the pro-coagulant cancer microenvironment is associated with increased fibrinolysis rates that simultaneously facilitate plasmin-dependent activation of latent TGF-β and, in conditions of high fibrinolysis rates, plasmin-dependent activation of TGF-β might become the predominant activation mechanism of TGF-β cytokine, as was shown in a case of gastric cancer [15]. The gene discussed is TGFB1; the disease is gastric cancer.