Results by multiple groups have converged on deciphering the role of CaM's two main targets that underlie and define the main calmodulinopathy phenotypes, i.e., Cav1.2 and RyR2, encoded by CACNA1C and RYR2, genes with a previously established role in LQTS and CPVT pathogenesis, respectively. Here, CACNA1C is linked to catecholaminergic polymorphic ventricular tachycardia.