Depending on the OV and cancer model, the mechanistic underpinnings associated with OV-MTA therapy efficacy and benefit included the potentiation of viral infection through perturbations to the translation (and thus expression of the protein products) of IFN or antiviral genes [194,195], increased expression of the cellular receptor employed by the virus [177], or the potentiation of cytostatic and cytotoxic phenomena, including mitotic slippage [186,190], apoptosis [168,169,186,191], autophagy [193], and immunogenic cell death (ICD) [192,193]. The gene discussed is IFNA1; the disease is cancer.