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A-T research is "A work in progress".

When an Israeli-led team of researchers cloned the gene for the rare ataxia telangiectasia syndrome in the summer of 1995, some likened the discovery to finding the Rosetta stone that helped archaeologists decipher Egyptian hieroglyphics. With the gene, they said, scientists now had a powerful tool to go back into A-T cells and decipher the molecular interactions that produce the syndrome. Years of research have strongly suggested that the syndrome will also yield new clues to some of today's hottest issues in biology and medicine such as DNA repair, programmed cell death, the workings of immune cells, neurologic deterioration, and cancer. Fourteen months later, researchers find themselves still in the early stages of learning how to use their Rosetta stone. They are tallying up all the possible mutations in the gene, debating where the A-T protein localizes in cells, and hammering out new research tools to work with the large A-T gene. "You've caught us a little early," said Pat Concannon, Ph.D., a scientist at the Virginia Mason Research Center in Seattle. "A-T is very much a work in progress." As such, A-T offers a glimpse into how the cloning of a gene energizes research on rare diseases, bringing an influx of new faces and ideas into the field. But it also shows how long-time A-T researchers, many of whom have dedicated much of their careers to tracking down the A-T gene, must now shift gears and enter unfamiliar research terrain — or be left in the dust. "When I got into the positional cloning studies, we basically left everything else behind and became molecular geneticists," said Richard Gatti, M.D., a scientist at the University of California at Los Angeles, who has studied A-T for about 30 years. "Now we have to become cell biologists. The genetics is done."