The sense that I got from the article was that the gene and protein were both normal components of all cells, and that the elevated levels of the protein was the agent that promoted cancer cell growth. I didn't see that they said the the gene or the protein were a mutation, but that the protein was a mutagen, causing cells to behave as cancer cells.
That seems kind of speculative, but I didn't do the research or read anymore than this article. It is an interesting concept, as is your work in anti-angiogenesis with thalidomide (how many hoops did you have to jump through to be allowed to try that?). They seem to be closely related in the growth of blood supply and the ultimate goals.
Have you ever investigated CFS (chronic fatigue syndrome) patients and the re/dox of their cellular activity? It seems to be the exact opposite of this research on the gene and protein in the article and your own work. I wonder if this could be the flip side of the same cellular activity, the lowered activity state, instead of the raised one that leads to cancer.