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It is a shame that grammar leaves no fossils behind. Few things have been more important to our evolutionary history than language. Because our ancestors could talk to each other, they became a powerfully cooperative species. In modern society we are so submerged in words—spoken, written, signed, and texted—that they seem inseparable from human identity. And yet we cannot excavate some fossil from an Ethiopian hillside, point to a bone, and declare, “This is where language began.”

Lacking hard evidence, scholars of the past speculated broadly about the origin of language. Some claimed that it started out as cries of pain, which gradually crystallized into distinct words. Others traced it back to music, to the imitation of animal grunts, or to birdsong. In 1866 the Linguistic Society of Paris got so exasperated by these unmoored musings that it banned all communication on the origin of language. Its English counterpart felt the same way. In 1873 the president of the Philological Society of London declared that linguists “shall do more by tracing the historical growth of one single work-a-day tongue, than by filling wastepaper baskets with reams of paper covered with speculations on the origin of all tongues.”

A century passed before linguists had a serious change of heart. The change came as they began to look at the deep structure of language itself. MIT linguist Noam Chomsky asserted that the way children acquire language is so effortless that it must have a biological foundation. Building on this idea, some of his colleagues argued that language is an adaptation shaped by natural selection, just like eyes and wings. If so, it should be possible to find clues about how human language evolved from grunts or gestures by observing the communication of our close primate relatives.


This line of thinking raised an exciting possibility: Perhaps language left a fossil record after all—not in buried bones, but in our DNA. Yet for years biologists could not find a single gene involved in language.

Ten years ago, that finally changed. In 2001 a team of British scientists announced the discovery of a gene, called FOXP2, that seems to be essential for language. FOXP2 came to light through the study of a family that had unusual difficulties with words. The KE family—so called in scientific papers for privacy reasons—lived in West London and included nine siblings, some of whom attended the same special speech and language school. Psychologists at the school discovered that four of the children struggled with language in a similar way. The meaning of sentences sometimes confused them: They might misinterpret “The girl is chased by the horse” to mean “The girl is chasing the horse.” They also had trouble speaking—dropping some sounds off the beginning of words, for example, so that they would say “able” when they meant “table.”

In 1987 the school headmistress referred the case to the Institute of Child Health at University College London. There, neurologists found that some of the children’s cousins had the same language troubles, as did some of the parents. Geneticists traced the condition to a grandmother and deduced that she probably carried a rare mutation that she had passed along. The mutation did not alter intelligence or psychological well-being; the KE family was normal in those regards. Its effects were limited to language—but within that narrow sphere, its effects were profound.

The family then came to the attention of geneticists at Oxford, who began a dogged search for the gene that caused these problems. They compared the DNA of family members, looking for distinctive markers shared only among the ones who had trouble with language. Among those with the language deficit, they found shared markers in a single region of chromosome 7. Years later, the scientists received a vital new clue when the same kind of language disorder was identified in an unrelated 5-year-old boy. He had experienced a particularly dramatic mutation, in which a piece of chromosome 5 had been swapped with a piece of chromosome 7. One end of the boy’s swapped DNA lodged itself in the same region that the Oxford team had identified in the West London family, right in the middle of the FOXP2 gene.