To further investigate the mechanism behind how the combination of HDACi and oHSV enhances virus replication, the expression of IFN-β- and IFN-induced signal transducers and activators of transcription 1 (STAT1), as well as IFN-stimulated genes (ISGs) protein kinase-R (PKR), and promyelocytic leukemia (PML), were evaluated in both glioma and squamous cell carcinoma cells. This evidence concerns the gene STAT1 and squamous cell carcinoma.