It has a broad cancer cell tropism and is effective when administrated intravenously in several murine tumor models, which is hypothesized to be associated with its vulnerability to the interferon pathway.22,23,24,25 A mutation in the M protein of the virus (VSVΔ51) enhances this vulnerability resulting in improved tumor-cell selectivity.26 Plaque forming assay on cancer cells demonstrated aptamers' ability to recover viral infectivity in the presence of rabbit serum containing neutralizing anti-VSV antibodies. The gene discussed is MYOM2; the disease is cancer.