Thus, the role of LV during tumor growth seems to be a complex process, involving on one hand the expression of different proteins by LECs that dampen antigen-specific CD8+ T cell response and metastasis (80, 84), and on the other hand tumor cells actively secrete VEGF-C to modulate LV function, promoting lymph leakage that blocks APC traveling to draining lymph nodes in order to initiate a strong adaptive immune response, and promotes an intratumoral M2 polarization environment that reduces local anti-tumoral response, allowing tumor growth. Here, VEGFC is linked to neoplasm.