Electrophysiological remodeling, i.e., reactivation of fetal cardiac genes, including T-type Ca2+ channel and hyperpolarization-activated, cyclic nucleotide-sensitive (HCN) cation channels (HCN2 and -4) have also been reported to increase the vulnerability to arrhythmia [6, 7]. Here, HCN2 is linked to cardiac arrhythmia.