Major mechanisms of resistance to anti‐VEGF therapy with Bev include activation of alternate pathways by pro‐angiogenic factors such as HGF, fibroblast growth factor, and Ang‐226, 27; selection of malignant cells showing resistance to anti‐VEGF therapy‐induced hypoxia, leading to increased invasion and metastasis7, 28; and increased tumor vessels with inherently low sensitivity to VEGF inhibition.29, 30. Here, VEGFA is linked to neoplasm.