In our MC38 tumor model, we observed that diminution of these myeloid precursors in mice treated with fruquintinib was concomitant with impaired tumor vascularization, suggesting that this drug can prevent tumor angiogenesis and lymphangiogenesis not only through direct inhibition of VEGFR3/FLT4/CD310 signaling in endothelial cells, but also by inhibiting macrophage polarization to M-LECPs and their incorporation into endothelial sprouts under angiogenic contexts. This evidence concerns the gene FLT4 and neoplasm.