Previous studies have reported modest reductions in RyR2 inhibition [80,133] but no changes in SK3 channel regulation [31], while the broad expression of CaM suggests that extra-cardiac manifestations may also occur, as evidenced by distinct neuronal phenotypes of arrhythmia-associated CaM variants in C. elegans [134]. The gene discussed is KCNN3; the disease is cardiac arrhythmia.