Efforts have already been undertaken to engineer SeV for a tumor application, but in contrast to our strategy, the so far reported anticancer effect was limited twofold: (i) it was dependent on the secretion of tumor cell-specific proteases such as urokinase-type plasminogen activator [24], [25] or matrix metalloproteinases [23], and (ii) spread of viruses did only occur by fusion events with neighboring cells due to a lack of progeny release via the cellular membrane. This evidence concerns the gene PLAU and neoplasm.