Earlier data suggested the role of CaM in regulating the cardiac Na channel (Nav1.5) inactivation, and a specific defect in Nav1.5 inactivation (increased persistent Na current) occurs in LQTS.7 Nav1.5 channels interact with CaM via an IQ motif on their C-terminus, independent of Ca2+, and play a crucial role in arrhythmogenesis.8 Unlike CaV1.2 channels, this interaction doesn’t trigger conformational changes. The gene discussed is CALM1; the disease is familial long QT syndrome.