As shown in Figure 1, because BDNF–TrkB promotes VEGF via PLCγ/PKCα and HIF−1α in human chondrosarcoma, VEGF, HIF−1α, and microvessel density are rational proxies for TrkB−axis output relevant to osteosarcoma vasculature and immune trafficking (54–56). This evidence concerns the gene NTRK2 and osteosarcoma.