In a broader sense, the multiple compensatory angiogenic factors/signaling pathways that tumors employ during anti-VEGF stress (Figures 1 and 2,) can be conveniently categorized as VEGF-dependent pathways, VEGF-independent signaling, mechnisms involving myeloid/stromal/tumor cell interactions and angiogenesis-independent vascular remodeling processes such as vessel cooption, intussusceptions and vascular mimicry. This evidence concerns the gene VEGFA and neoplasm.