The importance of IFNs in control of tumors is evident from the findings that mice lacking functional IFN systems are more prone to spontaneous tumor development and increased tumor burden in experimental models (4–6) as well as from the fact that loss-of-function mutations become enriched in genes coding for central mediators of the IFN system during tumor development (e.g., in the case of melanoma) (7, 8) indicating a pronounced selection pressure elicited by the IFN system. Here, IFNA1 is linked to neoplasm.