In BRAF‐mutant mouse models, we demonstrate that although targeted inhibition of either BRAF or VEGF initially suppresses the growth of BRAF‐mutant tumors, combined inhibition of both pathways results in apoptosis, long‐lasting tumor responses, reduction in lung colonization, and delayed onset of acquired resistance to the BRAF inhibitor PLX4720. The gene discussed is VEGFA; the disease is neoplasm.