Ji M. Quigg et al. designed a NAT-expressing ICP5.1716 null mutant (HSV-1) of HSV34.5, named HSV1716/NAT, and introduced the NAT gene into glioma cells using plasmid-mediated transfection to explore the feasibility of a combined therapeutic approach for glioma treatment with HSV1716/NAT and [131I]MIBG in in vitro experiments [13]. The gene discussed is BRD2; the disease is glioma.