Umezu et al. demonstrated that exosomes derived from multiple myeloma cells can transfer miR135b to endothelial cells to directly suppress factor-inhibiting hypoxia-inducible factor 1 (FIH-1), and activate HIF-1α via the HIF-FIH signaling pathway, leading to the overproduction of angiogenic cytokines such as VEGF, angiopoietin-1, and osteopontin, therefore resulted in endothelial cell migration, proliferation, and angiogenesis [50]. The gene discussed is HIF1A; the disease is plasma cell myeloma.