As functional L-type Ca2+ channel changes represent a disease mechanism of atrial fibrillation, major future questions are how Cav1.2 and Cav1.3 clusters are organized locally and relatively to RyR2 channel Ca2+ release sites, and which specific voltage-dependent roles the atrial L-type Ca2+ channel isoforms exert in A-tubules. The gene discussed is CACNA1C; the disease is atrial fibrillation.