In fact, VEGFR3 signaling in macrophages influences their plasticity from pro-inflammatory (M1-like) to anti-inflammatory (M2-like) phenotypes (14) and M-LECPs contribute to tumor lymphangiogenesis and immune modulation making them a unique target to impair lymphatic metastasis and myeloid-driven immunosuppression (15). This evidence concerns the gene FLT4 and neoplasm.