The pacemaking function of Cav1.3 in the sinoatrial node and its absence in the ventricular myocardium predict Cav1.3‐selective inhibitors as bradycardic agents lacking relevant negative inotropy (Mangoni et al., 2003; Sinnegger‐Brauns et al., 2004a) with therapeutic potential in heart failure. This evidence concerns the gene CACNA1D and heart failure.