Researchers have long understood that Kabuki syndrome—a genetic disorder causing intellectual disability—stems from mutations in genes that help keep DNA accessible for reading. What has remained elusive is how to fix it. A new study in mice suggests the answer might lie not in a pill, but in a diet.

A new mouse model for Kabuki Syndrome, created using a specific genetic change found in a patient, reveals that some core symptoms may arise independently of the enzyme activity typically lost in the condition. (1, 48) This model, which carries a "missense" variant—a single-letter change in the DNA code—recapitulates many physical features of the syndrome but intriguingly spares the brain from certain neurological deficits seen in earlier models. (5, 7, 44)