This combinational strategy has the potential to overcome the resistance to antiangiogenic monotherapies targeting exclusively the VEGF pathway because poor responses to these therapies are driven by the upregulation of alternative proangiogenic pathways, increased protective pericyte coverage of tumour blood vessels and the recruitment of proangiogenic myeloid inflammatory cells, including MDSCs to tumours [297]. The gene discussed is VEGFA; the disease is neoplasm.