In contrast, our in vivo study reveals a preponderance of the mutant versus wild-type CALM protein in hearts from mice heterozygous for the Calm1N98S allele, suggesting that a high mutant–to–wild-type CALM ratio counterbalances the relatively low potency of N98S-CALM in inducing an arrhythmia phenotype. This evidence concerns the gene CALM2 and cardiac arrhythmia.