PreXMRV1 was shown to be present as an ERV in samples from the mouse with the xenograft. The source for preXMRV2 was never identified. The argument that it must have been present, because it came out in the form of XMRV was circular. This would be true whether it came from an ERV in a mouse or arrived as an active retrovirus in either mice or humans. An active retrovirus is much more likely to recombine with similar ERVs. This changes the probabilities of origin considerably. Instead of a single mouse in a single experiment we now have to consider the probability of recombination in every mouse with both the ERV and an active infection. This study strongly suggests there is such an active retrovirus in mice, and it is young, not ancient. Sequence homology points to a mixture of polytropic and xenotropic strains, as reported in other cases. We won't know the actual tropism until we have the complete virus to study. In particular we need to know the envelope to determine how it enters cells. There is good reason to believe it can use XPR1 receptors, which humans have, but most mice lack. The story is not over.