Parallels can be made with studies of variants in SCN5A cardiac sodium channel and the β subunits of Nav1.5 in infants who die from SIDS.38, 39 Functional variants in these genes can predispose patients to cardiac arrhythmia but they are also rarely found in the Exome Aggregation Consortium database, indicating that they contribute to the probability of death occurring but might not define it.40 This evidence concerns the gene SCN5A and sudden infant death syndrome.