The experimental data from the present study indicate that anlotinib-mediated abrogation of VEGFR-3 and subsequent activation of its downstream effectors (i.e., Erk and Akt30) in LECs blocks lymphangiogenesis during benign lymphangioma development and tumor progression through lymphatic vessels, because the incidence of lymph node metastasis was decreased by anlotinib treatment in a mouse model of lung cancer. The gene discussed is FLT4; the disease is neoplasm.