Recent advances extending our knowledge of how to best harness the immune system to mount an anticancer response through enhanced T-cell activation have shifted focus towards the use of virotherapies expressing immune checkpoint inhibitors and/or bispecific T-cell engagers (BiTEs), designed to be secreted from virally infected cells, and physically “bridge” the T-cell to tumour cells via a suitable bispecific fusion molecule (for example, a bi-specific anti CD3-anti CD19 molecule). The gene discussed is CD19; the disease is neoplasm.