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This article discusses a study that investigates the role of the Scn1b gene in cardiac energetics. The researchers focused on mice lacking Scn1b and examined if these mice had compromised mitochondrial energetics. The results showed that the loss of the β1 subunit in the heart led to decreased mitochondrial respiration and increased reverse electron transport. These findings suggest that targeting mitochondrial deficits could be a potential therapeutic approach for reducing the risk of cardiac arrhythmias and cardiovascular disease in individuals with Scn1b mutations. [Extracted from the article]