The possibility of EC differentiation directly from malignant tumor cells has been proposed in lymphoma, myeloma, chronic myeloid leukemia (CML), breast cancer, neuroblastoma, and glioblastoma.24–26 These alternative mechanisms to generate tumor vessels perhaps explain the largely ineffective outcome of clinical trials in which antiangiogenic agents (generally targeting VEGF-A) are used in conjunction with chemotherapy. This evidence concerns the gene VEGFA and lymphoma.