In our hands, treatment with the VEGFR3/FLT4/CD310 inhibitor fruquintinib as a single agent reshaped the tumor’s immune landscape by incrementing the amount of CD4+ and CD8+ T lymphocytes, and more importantly, the amounts of immature monocytes (Ly6C+) while it reduced the percentages of differentiated myeloid populations, including M2-like (CD206+) macrophages and type II dendritic cells (cDC2). The gene discussed is FLT4; the disease is neoplasm.