ERBB2 and neoplasm: The self-origin of such tumor associated antigens (e.g., HER2) increases the potential risk of deleterious on-target, off-tumor toxicity; for these reasons, we recently published a proof-of-concept of dual restriction by combining the retargeting to HER2 to replicative conditioning to cancer cells by the SurE_oHSV hosting surviving promoter driving ICP4 expression [7].