Moreover, inhibition of cancer antiviral defenses, specifically RNAseL and PKR, resulted when cancer cells were exposed to sunitinib, a multi-tyrosine kinase inhibitor originally developed as an inhibitor of VEGF-R and PDGF-R signaling, yielding strong anti-tumor synergy with IFN-sensitive oncolytic VSV [132]. The gene discussed is EIF2AK2; the disease is neoplasm.