Similar to sodium current traces from Nav1.5 in transfected Xenopus oocytes, peak Na+ channel currents were reduced in iPSC-CMs from DCM patients with the SCN5a p.C335R variant (Figure 3B), showing that this mutation led to loss-of-function and decreased peak INa in patients with cardiac conduction disease and DCM in this family. This evidence concerns the gene SCN5A and familial dilated cardiomyopathy.