Transthyretin amyloid cardiomyopathy (ATTR-CM) is an increasingly recognized cause of heart failure (HF) resulting from the myocardial deposition of misfolded protein fibrils.1 Disease-modifying therapies for ATTR-CM, ATTR stabilizer and gene silencing pharmacotherapy have recently been developed.2,3 This has resulted in a clinical need for early detection and accurate quantitation of disease burden, prognosis, and response to treatment. This evidence concerns the gene TTR and heart failure.