CACNA1D and sinoatrial node dysfunction and deafness: Given that Cav1.3(α1D) knockout in mice is viable (Platzer et al., 2000; Zhang et al., 2005) and reproduces key aspects of the SANDD syndrome, future studies will need to characterize the yet unknown role of Cav1.3 LCCs in ATs and how AM function might be affected by knockout or SANDD mutations.