Since wild type HSV1 infection is known to stimulate mTORC1-dependent 4E-BP1 inactivation [25], our results suggest that dysregulated eIF4E/4E-BP ratio and/or hyperactivated mTORC1 in cancer cells contribute to sustain, and ultimately favor viral protein synthesis in the presence of asTORi over antiviral mRNA translation. Here, EIF4E is linked to infection.