In 1990, Geisterfer-Lowrance et al. reported the first evidence of a gene defect underlying a form of intrinsic heart-muscle disease. They found that a mutation in the gene encoding the contractile protein β-myosin heavy chain results in familial hypertrophic cardiomyopathy.¹ Since then, mutations in seven other genes, all encoding proteins of the myofibrillar apparatus, the fundamental contractile unit of the cardiomyocyte, have been found to cause familial hypertrophic cardiomyopathy.²,³ These proteins include sarcomeric proteins (ventricular myosin light chains 1 and 2, cardiac troponin I and T, α-tropomyosin, α-cardiac actin) and an intrasarcomeric cytoskeletal protein (myosin-binding protein C). Although the . . .