Many osteosarcoma tumors and metastases harbor p53 mutations or other mechanisms (e.g., MDM2 amplification) that interfere with apoptosis after damage from standard chemotherapy, newer agents such as tyrosine kinase inhibitors (TKI) of vascular endothelial growth factor (VEGF) (2, 3), and/or radiation therapy (4, 5). This evidence concerns the gene VEGFA and osteosarcoma.