The tumor specificity of RRV is ensured by the absolute requirement of cell division for active infection and virus-selective advantages in the tumor microenvironment related to blunted innate immune responses (e.g., APOBECs, DDX41, tetherin, TRIM-5α) [12,13,14,15], as well as suppressed acquired immune responses relative to normal cells [16,17,18]. Here, BST2 is linked to neoplasm.