It has been reported that the anti-VEGF monoclonal antibody bevacizumab induces intratumoral hypoxia, likely through excessive vessel remodeling (142), thus increasing the population of cancer stem cells (CSCs) in human breast cancer xenografts (143), and promoting epithelial to mesenchymal transition (EMT) in a murine model of bevacizumab-resistant pancreatic cancer (144). This evidence concerns the gene VEGFA and cancer.