Thus, in contrast to the “classical” mechanism of atrial arrhythmogenesis in AF involving reduced electrical conduction velocity and shortening of atrial APD and effective refractory periods (AERP) that perpetuate AF through promotion of electrical re-entry [24], we suggest that in HF patients treated with dapagliflozin, pharmacologic activation of K2P2.1 and K2P17.1 current levels may specifically counteract atrial remodeling and suppress atrial arrhythmias. The gene discussed is KCNK2; the disease is atrial fibrillation.