Therefore, if oNIS+BRD expression could be selectively regulated using an oncolytic virus for gene delivery, such as talimogene laherparepvec (T-Vec), a second-generation oncolytic herpes simplex virus type 1 (HSV-1) armed with GM-CSF [57,58], normal tissue with high endogenous NIS expression would be spared from unnecessary damage associated with increased iodine uptake, and damage induced by oNIS+BRD overexpression would be specific to cancer cells. Here, SLC5A5 is linked to cancer.