HDAC9 and atrial fibrillation: 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.