This is further supported by the identification of CaM mutations in patients with clinical presentations of mixed LQTS and CPVT phenotypes (e.g., the previously reported CaM D132E and Q136P mutations) [26], highlighting the fact that multiple factors can lead to defects in vital functions and interactions of this multifunctional Ca2+ sensor with RyR2 and the other ion channel complexes in the heart [36,37]. This evidence concerns the gene CALM2 and familial long QT syndrome.