Publishing their findings in the current issue of the Proceedings of the National Academy of Sciences, Virshup's group showed that cells with mutant CK1 genes introduced into them did make the PER protein disappear more quickly. Because of this, the clock ticked faster. "We never would have looked for it if it weren't for this mathematician," says Virshup.

"What this means is we now have a much clearer understanding of how the clock works," says Andrew Loudon an animal biologist at the University of Manchester in England.

Others are less convinced. "They could be right, but it's far from conclusive," says Liz Maywood at the University of Cambridge's Department of Physiology, Development and Neuroscience, in England. What is not clear, she says, is whether this effect has been caused by the mutation or whether it's due to the cells entering a particularly active phase of their natural clock cycle. "Some drugs can shift the phase of the clock," she says.

Virshup is dismissive of this, arguing that phase effects of the cells were unlikely to have influenced the experiments because of the conditions under which the cells were grown. "There are effects of circadian rhythms on cell cycles, but not the other way around," he says.

"Knowing what we now know, anyone setting out to develop drugs would be having a devil of a time," says Loudon. To the best of his knowledge, Virshup says, there are no drug therapies on the market based on the previous understanding of the tau mutation. But, he adds, at least two companies have been working on drugs based on our prevailing understanding of these CK1 mechanisms. "That may be why we haven't seen any approved drugs on the market yet," he says.