The hypothetical rationale for the resistance includes epigenic mechanisms of resistance, unresponsiveness of tumor vasculature to anti-VEGF agents [5], upregulation of alternative proangiogenic pathways, enhanced protection by pericytes, increased invasiveness of tumor cells into local tissue normal vasculature, metastatic seeding, and tumor cell growth in lymph nodes and distant organs, as well as failure of anti-VEGF agents in fully blocking all VEGF signaling pathways [120, 121]. The gene discussed is VEGFA; the disease is neoplasm.