CaM mutations which perturb modulation of these targets promote LQTS (Chazin & Johnson, 2020; Hussey et al., 2023; Jensen et al., 2018), the most common genetic aetiology of which arises from loss‐of‐function mutations in Kv7.1 (∼50% of cases) (Crotti et al., 2008; Schwartz et al., 2012). The gene discussed is CALM2; the disease is familial long QT syndrome.