TKT and neoplasm: We recently described a novel thymidine kinase (TK)-deleted, N1L gene-deleted VV, VVLΔTKΔN1L, which demonstrated potent gene-deletion-driven tumor specificity, activation of antitumor immunity and potent efficacy in a number of tumor models in vivo.13–15 Additionally, we have developed a platform to improve intravenous delivery of VV based on transient pharmacological inhibition of PI3 Kinase δ (PI3Kδ) to prevent uptake of the virus by macrophages, a major factor limiting systemic administration.16 This platform goes some way toward addressing the shortcomings of OVT identified above.