We demonstrate here that LQTS‐CaM mutants have the capacity to prolong membrane repolarisation, CaM mutants have also been demonstrated to perturb Cav1.2 inactivation and could modulate a range of arrhythmogenic substrates (Benitah et al., 2010; January et al., 1988; Madhvani et al., 2015; Weiss et al., 2010). Here, CACNA1C is linked to familial long QT syndrome.