SCN1A and Dravet syndrome: Here, in our DS model, altered Ca2+ handling downstream of reductions in Nav1.1 expression at the T-tubules may indirectly affect Nav1.5 function via changes in the binding of calmodulin to the channel or altered Ca2+-calmodulin dependent protein kinase-II-mediated channel phosphorylation, ultimately resulting in increased INa and arrhythmia [77,78].