One million exomes identify FNIP1 as a metabolic brake.

Loss-of-function variants in FNIP1, a mitochondrial energy expenditure suppressor, are linked to reduced cardiometabolic disease risk in over 1 million exomes.

• Why it matters: Understanding genetic factors that influence energy metabolism can reveal new targets for preventing or treating cardiometabolic diseases, which remain a major health challenge.
• What they did: Exome sequencing of more than 1 million individuals identified rare variants in FNIP1 associated with energy regulation, highlighting its role as a metabolic brake.
• The result: Inhibiting FNIP1 could serve as a targeted therapy to enhance mitochondrial energy expenditure and lower the risk of cardiometabolic conditions.