Recently, we generated CaV1.2 exon 33 specific knockout mice (exon 33−/−) and these exon 33-null mice were found to develop cardiac arrhythmia and dysfunction, owing to increased CaV1.2 channel currents arising from a leftward shift of voltage-dependent activation and inactivation potentials as compared to wild-type (WT) (exon 33+/+) cardiomyocytes.7 Here, CACNA1C is linked to cardiac rhythm disease.