Emerging evidence has demonstrated that the antiangiogenic agents not only normalize tumor vascular network, but modulate tumor immune microenvironment through various mechanisms, including promoting T-cell infiltration, inducing M1 macrophage polarization, decreasing the recruitment of Treg and myeloid suppressor cells, and downregulating inhibitory immune checkpoints such as PD-L1, thereby converting the tumor immune microenvironment from immunesuppressive to immune-active35–38. This evidence concerns the gene CD274 and neoplasm.