Power to demonstrate association will be limited for genes causing only a small proportion of DCM (eg, evidence of cosegregation of nontruncating variants in SCN5A with arrhythmogenic DCM is reported alongside functional data demonstrating altered sodium channel function20), or for genes in which variation in specific functionally important residues or genic subregions is disease-associated, but not detectable against background variation in other regions tolerant of variation. The gene discussed is SCN5A; the disease is familial dilated cardiomyopathy.