The double-strike PD-1/PD-L1 immune checkpoint inhibitor-like behavior of RSV based on its ability to directly target PD-L1 either via key post-translational modifications such as N-linked glycosylation [110–114] or via direct binding to PD-L1 to block PD-1 binding [71–77] interferes with PD-L1 stability and trafficking, impedes the correct targeting of PD-L1 to the cancer cell plasma membrane, and lastly elicits considerably enhanced cytotoxic T-lymphocyte immune-surveillance against tumor cells (Figure 9). Here, CD274 is linked to neoplasm.