Recent data suggest that, at least in certain tumor types, the angiogenic form of VEGF-D, identical or similar to the KLK3 activated VEGF-D, is responsible for the tumor becoming refractory to anti-VEGF-A treatment [122], and activated VEGF-C may rather act as a lymphangiogenic factor than an angiogenic one [72]. Here, VEGFC is linked to neoplasm.