The previous findings that an exogenous supply of type 1 IFNs restored the chemotherapeutic responses to DOX in Tlr3−/− but not IFN (α and β) receptor 2-deficient (Ifnar2−/−) sarcomas growing in mice,10 together with the ability of OVV-induced IFN-β in murine and human tumor cell cultures to augment responses to DOX,9 raised the possibility that IFN-β produced in response to OVV could enhance DOX-induced apoptosis mediated by CREB3L1 translocation to the nucleus. The gene discussed is IFNB1; the disease is sarcoma.