As VEGF/Nrp2 signaling sustains PD-L1 expression on tumor cells, inhibition of VEGF binding via Nrp2-specific monoclonal antibodies (aNRP2-10/humanized and aNRP2-28/mouse) in neuroendocrine prostate cancer organoids and syngeneic prostate cancer mouse models resulted in decreased PD-L1 expression on tumors and increased immune infiltrate and immune-mediated tumor cell killing, while regressing tumors in vivo [110]. The gene discussed is NRP2; the disease is prostate carcinoma.