Previous studies reported that a PITX2+/−-deficient condition modulated atrial resting membrane potentials and increased both AF susceptibility and the efficacy of AADs, especially class IC drugs (Syeda et al., 2016; Bai et al., 2021) and that dronedarone restored the action potential of myocytes affected by hERG mutations to that of wild-type (WT) myocytes (Loewe et al., 2014). Here, PITX2 is linked to atrial fibrillation.