The molecular mechanisms underlying the two main phenotypes has largely been ascribed to specific dysregulation of the two primary cardiac Ca2+ channels, CaV1.2 for LQTS, and RyR2 for CPVT-like phenotypes (Limpitikul et al., 2014; Yin et al., 2014; Søndergaard et al., 2019; 2020; 2017; Nyegaard and Overgaard, 2019; Holt et al., 2020). Here, CACNA1C is linked to familial long QT syndrome.