Thus, our findings that SOX2-OE enhances the oncomodulatory phenotypes of HCMV, a phenotype that can be reversed by increasing PML expression strongly argue for a role for the SOX2-PML axis in the regulation of HCMV infection in vivo and potentially, a mechanism that can account for the contribution of HCMV to the malignant phenotype of GBMs. Here, SOX2 is linked to cytomegalovirus infection.