For the clinical development of VSV32, we overexpressed the IFNβ gene in the virus25 to enhance safety (increased antiviral IFN expressed in normal cells) and to increase the immunogenicity of infected/dying tumor cells, as IFNβ acts as a key signal 3 cytokine to facilitate priming of tumor-reactive T cells25,32,33. The gene discussed is IFNA1; the disease is neoplasm.