Probably, thanks to the multiplicity and intrinsic redundancy of ion channels in the cardiac pacemaker, our work showed that inhibition of SK4 K+ channels rescues in vitro the cardiac arrhythmias exhibited by hiPSC‐CMs derived from CPVT2 patients carrying the CASQ2 D307H mutation and by SAN cells isolated from CASQ2‐D307H KI mice. This evidence concerns the gene KCNN4 and cardiac rhythm disease.