As tumor lymphangiogenesis via maspin seems to be rather modulated by VEGF-C and its receptors VEGF-R2 and VEGF-R3 [14] and by the Hipoxia-inducing factor (HIF-1α) [62], while systemic metastases mainly occur via VEGF-A [63,64], the maspin-based tumor therapeutics should target these specific molecular endpoints. The gene discussed is VEGFC; the disease is neoplasm.