Truncating TTN mutations are a good example, as evidence is accumulating regarding changes in the cardiac metabolism and energy homeostasis.49 The increase in the energy metabolism could be a mechanism of metabolic compensation for the sarcomere insufficiency.50 This change in metabolism related to truncating TTN mutations can be a valid downstream target for intervention to prevent disease onset toward DCM. The gene discussed is TTN; the disease is familial dilated cardiomyopathy.