This defect was the combined result of prolonged elevated expression of Dlk1, causing a failure of BAT differentiation and consequently reducing expression of β-adrenergic receptors, and hypothyroidism due to misregulation of Dio3. Our results show that small coordinated alterations in imprinted gene dosage in the context of a cluster have a major impact on postnatal survival. Here, DIO3 is linked to hypothyroidism.