LQTS‐associated CaM variants have been shown to perturb a range of other cardiac ion channels, including reducing the Ca2+‐dependent inactivation of Cav1.2 (Gomez‐Hurtado et al., 2016; Limpitikul et al., 2014; Prakash et al., 2023; Yin et al., 2014), altered inhibition of RyR2 (Nomikos et al., 2014; Vassilakopoulou et al., 2015) and activation of CaMKIIδ (Berchtold et al., 2016; Prakash et al., 2023). The gene discussed is CACNA1C; the disease is familial long QT syndrome.