However, while several modes of VEGF redistribution, such as through MMP9, heparinases, or VEGF inhibitor cleavage are implicated as pro-tumorigenic, mediating an angiogenic switch [15,16,19,20,29,30,32], there are several notable exceptions where protease activity instead leads to diminished tumor growth [7], an effect similar to the plasmin-mediated loss of wound healing due to a loss of angiogenesis [75]. The gene discussed is PLG; the disease is neoplasm.