Malignant peripheral nerve sheath tumors (MPNSTs) were observed to resist infection of oncolytic HSV-1 through activation of the janus kinase (JAK)/signal transducer and activator of transcription 1 (STAT1) signaling pathway that drives constitutive expression of IFNs and resultant IFN-stimulated genes to diminish virus reproduction, as a result, co-treatment with the JAK inhibitor ruxolitinib improved the susceptibility of MPNSTs to oncolytic HSV-1 and showed superior antitumor activity over monotherapy [88, 89]. Here, STAT1 is linked to infection.