Right now, the jury is still out on STAP cells. It is not known for sure if STAP (stimulus-triggered acquisition of pluripotency) is a genuine phenomenon. Top laboratories around the world, in Japan, the United States and elsewhere, are working to try to replicate the findings of Obokata et al. (Nature 505:641-647; Nature 505:676-680). As they do this, I sincerely hope they take the sage advice of Hans Scholer, who suggested that RIKEN (the main team who is attempting to replicate the work) involve Obokata in each and every step of the procedure (see Nature 508:299). Obokata insists that STAP is real. This may be the case, and it may be that the procedure is very tricky; she might have succeeded where others have failed because she has apparently spent every waking moment for years working out the details. This is our (the scientific community's) chance to really get to the bottom of this issue. If we blow this opportunity, we may never know the answer to this important question. If we're not careful, this moment could pass us by.

The reason why it is so important to know if STAP is real is because, if it is, then this will be a paradigm-shifting discovery. In the 1990s (and even earlier, through the work of Sir John Gurdon) we learned that the cytoplasm of an enucleated oocyte can reprogram a nucleus from a terminally-differentiated somatic cell that has been transferred into it (using somatic cell nuclear transfer, SCNT) to a plurpotent state. More recently, in 2006, we learned that a limited set of four factors, the so-called Yamanaka factors, can also reprogram somatic cells to pluripotency, producing iPS cells. These were astounding discoveries, ones that told us something remarkable about the nature of the cell: that it has the capacity to "reverse course" and become a pluropotent stem cell under certain conditions. If STAP is real, then this means that the conditions under which this sort of thing can occur are even broader than we ever could have imagined, to also include external triggers (low pH, mechanical stress). What would this tell us about nuclear-cytoplasmic interaction and the role of the whole cell in gene expression patterns? How would the human body (for instance) normally prevent this kind of reversion to pluripotency, which would potentially lead to cancer? These are exciting questions. Let's get this thing right; let's pursue all avenues to find out what the real answer is!

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