Indeed, it has been demonstrated that two types of “bystander tumor cell killing” mechanisms are mediated by this approach: (a) a “direct” bystander effect, due to the transfer of ganciclovir triphosphate from HSV-TK-positive tumor cells into untransfected neighboring cells [12–14], (b) a systemic immunologically-mediated bystander effect due to the in vivo immune presentation of tumor-specific/associated antigens following the killing of HSV-TK—expressing cells [15, 16]. This evidence concerns the gene TKT and neoplasm.