Enhancement of Kcnn1 mRNA transcript levels by genetic inactivation of Hdac9 or suppression of Kcnn1 following knockdown of Hdacs2, 3, 6, and 7 provide the mechanistic basis for individualized management of distinct AF disease stages that are characterized by increased‐ or decreased KCa2.1 channel abundance and inverse changes in atrial APD, respectively. Here, KCNN1 is linked to atrial fibrillation.